目录号 | 产品详情 | 靶点 | |
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T37844 | |||
Kigamicins are natural antitumor antibiotics that selectively kill pancreatic cancer PANC-1 cells only under nutrient-starved conditions. They also show antimicrobial activity against Gram-positive bacteria, including methicillin-resistant S. aureus. Kigamicin C inhibits PANC-1 cell survival in nutrient-deprived media at a 100-fold lower concentration than that required for cells maintained in nutrient-rich media. A related compound, kigamicin D, is active in vivo, suppressing the tumor growth of several pancreatic cancer cell lines in nude mice. It blocks the activation of Akt induced in PANC-1 cells placed in nutrient-deprived media. Kigamicin can also induce necrosis in human myeloma cells, but not normal lymphocytes, maintained in nutrient-rich media (CC50 = 100 nM). | |||
T71293 | |||
Nifuroxazide-d4 is intended for use as an internal standard for the quantification of nifuroxazide by GC- or LC-MS. Nifuroxazide is a nitrofuran antibiotic. It is active against strains of the enteropathogenic bacteria C. jejuni, Salmonella, Y. enterocolitica, Shigella, and E. coli. It inhibits quorum sensing and virulence factor production in P. aeruginosa. Nifuroxazide inhibits STAT3 activity in a reporter assay and decreases viability of U266 and INA-6 myeloma cells, which have constitutive STAT3 phosphorylation, with EC50 values of approximately 4.5 µM for both. It also decreases viability, migration, and invasion of, and induces apoptosis in, MCF-7, 4T1, and MDA-MB-231 breast cancer cells. Nifuroxazide reduces tumor growth and prevents pulmonary metastasis in a 4T1 murine mammary carcinoma model. It also reduces diarrhea, weight loss, and colon inflammation in a rat model of acetic acid-induced ulcerative colitis. | |||
T81942 | |||
Lenalidomide (sodium)是Thalidomide的衍生物,这种口服活性的免疫调节剂通过分子胶模式作用。作为泛素E3连接酶cereblon(CRBN)的配体,Lenalidomide (sodium)通过CRBN-CRL4泛素连接酶复合体,针对淋巴转录因子IKZF1和IKZF3进行选择性泛素化和降解。此外,Lenalidomide (sodium)有效抑制成熟B细胞淋巴瘤的增长,如多发性骨髓瘤,并能促使T细胞分泌白细胞介素-2(IL-2)。 | |||
T21763 | |||
Lenalidomide hydrochloride (CC-5013 hydrochloride) 是 Thalidomide 的衍生物,也是一种具有口服活性免疫调节剂,以分子胶的方式作用。Lenalidomide hydrochloride (CC-5013 hydrochloride) 是一种泛素 E3 连接酶 cereblon (CRBN) 的配体,通过 CRBN-CRL4 泛素连接酶对两种淋巴转录因子 IKZF1 和 IKZF3 进行选择性泛素化和降解。Lenalidomide hydrochloride (CC-5013 hydrochloride) 特异性抑制成熟 B 细胞淋巴瘤 (包括多发性骨髓瘤) 的生长,并诱导 T 细胞释放白细胞介素-2 (IL-2)。 | |||
T80919 | |||
Tumour-associated MUC1 epitope是一种具有标志性的生物活性肽。作为高度糖基化的I型跨膜糖蛋白MUC1的一部分,该肽通过特定的胞外结构域展现,该结构域包含20个氨基酸组成的可变数量串联重复序列(VNTR)。在多种人类腺癌及血液恶性肿瘤(如多发性骨髓瘤和B细胞淋巴瘤)中细胞表面表达过量,因此,MUC1是许多免疫治疗策略的关键靶点。 | |||
T71252 | |||
PC-046 is a potent tubulin-binding agent, which was originally identified for development based on selective activity in deleted in pancreas cancer locus 4 (DPC4/SMAD4) deficient tumors. PC-046 has growth inhibitory activity in a variety of tumor types in vitro, and efficacy in SCID mice was shown in human tumor xenografts of MV-4-11 acute myeloid leukemia, MM.1S multiple myeloma, and DU-145 prostate cancer. Pharmacokinetic studies demonstrated relatively high oral bioavailability (71 %) with distribution to both plasma and bone marrow. No myelosuppression was seen in non-tumor bearing SCID mice given a single dose just under the acute lethal dose. The COMPARE algorithm in the NCI-60 cell line panel demonstrated that PC-046 closely correlated to other known tubulin destabilizing agents (correlation coefficients ≈0.7 for vincristine and vinblastine). Mechanism of action studies showed cell cycle arrest in metaphase and inhibition of tubulin polymerization. Overall, these studi...... | |||
T83786 | |||
8-Chloroadenosine-5’-triphosphate(8-chloro ATP)是抗癌剂8-chloro cAMP的活性代谢物,也是核苷酸腺苷5’-三磷酸(ATP)的衍生物。它通过8-chloro cAMP、8-chloroadenosine以及一磷酸和二磷酸中间体形成。应用8-chloro cAMP或8-chloroadenosine后,8-chloro ATP可累积长达12小时,与细胞生长抑制、内源性ATP水平下降以及患者源多发性骨髓瘤细胞中RNA合成减少(但DNA合成不受影响)相关。在1.5至8 mM浓度范围内,它抑制topoisomerase II-α依赖的超螺旋pUC19 DNA放松,同时在1 mM时减少了K562人髓性白血病细胞中topoisomerase II-α催化的ATP水解50%。 | |||
T83867 | |||
UNC8153 是一种 NSD2(组蛋白-赖氨酸 N-甲基转移酶)的降解剂,其通过诱导NSD2的降解,具有350 nM的50%降解常数(DC50)值,并且在20 µM浓度下对NSD2具有选择性,而不选择NSD1和NSD3。在MM.1S多发性骨髓瘤细胞中,UNC8153 (10 µM) 能够诱导NSD2降解并减少组蛋白H3赖氨酸36位二甲基化(H3K36me2),这一效应可以被泛素激活酶抑制剂MLN4924所抑制。它减少了表达带有在1099位上谷氨酸到赖氨酸激活突变的NSD2(NSD2E1099K)的MM.1S细胞的增殖,但在20 µM浓度下,对表达野生型NSD2的MDA-MB-231、U2OS或HEK293细胞无效。UNC8153 (20 µM) 降低了在迁移实验中MM.1S细胞的附着能力。 | |||
T36574 | |||
GW841819X is an analogue of (+)-JQ1 and a novel inhibitor of BET bromodomains. GW841819X was a single enantiomer but of undefined chirality at the 4-position of the benzodiazepine ring3. GW841819X and JQ1 were recently discovered that bind to the acetyl-lysine binding pocket of BET bromodomains with Kd ranges from 50 to 370 nM [1]. GW841819X bounded to both the individual BD1 and BD2 domains with affinities of 46 and 52.5 nM, respectively. GW841819X-Brd3 interaction was estimated to be around 70 nM4. GW841819X displayed activity in vivo against NUT-midline carcinoma, multiple myeloma, mixed-lineage leukemia, and acute myeloid leukemia1. It also potent induced the ApoA1 reporter gene with an EC50 of 440 nM. It had very little effect on LDL-R luciferase activity at the concentrations at which it induces ApoA1 expression, suggesting that the effect is indeed specific3. GW841819X competed directly with GATA1 site for BD1 binding and also specifically blocked the interaction between Brd3 and acetylated GATA14. Recent findings reported that GW841819X are chose as an interest compound to further develop into potential drugs against diseases including cancer, HIV infection and heart disease2. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04730 | LAG-3 Protein, Human, Recombinant (His) | Human | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-04939 | LAG-3 Protein, Human, Recombinant | Human | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-05092 | LAG-3 Protein, Cynomolgus, Recombinant (74 Pro, His) | Cynomolgus | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-05319 | BCMA/TNFRSF17 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-04493 | BCMA/TNFRSF17 Protein, Human, Recombinant (rFc) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-05568 | BCMA/TNFRSF17 Protein, Human (His & hFc), PE conjugated | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-03213 | BCMA/TNFRSF17 Protein, Rhesus, Recombinant (hFc) | Rhesus | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-01257 | uPAR/PLAUR Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Urokinase plasminogen activator (uPA) and/or its receptor (uPAR) are essential for metastasis, and overexpression of these molecules is strongly correlated with poor prognosis in a variety of malignant tumours. uPAR and uPA levels in both resected tumor tissue and plasma are of independent prognostic significance for patient survival in several types of human cancer. This system has classically been thought to drive tumor progression by mediating directed extracellular proteolysis on the surface of migrating or invading cells, and intervening with this proteolysis by targeting uPAR has been proposed to represent a novel approach for inhibiting tumor progression. uPAR, also known as PLAUR or CD87, has been implicated in the growth, metastasis, and angiogenesis of several solid and hemotologic malignancies. uPAR is a highly glycosylated, 55-60kDa integral membrane protein linked to the plasma membrane by a glycosylphosphatidylinositol (GPI) anchor. It is part of a cell surface system that also consists of the serine protease uPA and several specific inhibitors (plasminogen activator inhibitors 1 and 2). Additionally, the analysis of CD87 (urokinase-type plasminogen activator receptor - uPAR) expression has a potential role in the diagnostic or prognostic work-up of several hematological malignancies, particularly acute leukemia and multiple myeloma.
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TMPY-02141 | uPAR/PLAUR Protein, Human, Recombinant (His) | Human | HEK293 | ||
Urokinase plasminogen activator (uPA) and/or its receptor (uPAR) are essential for metastasis, and overexpression of these molecules is strongly correlated with poor prognosis in a variety of malignant tumours. uPAR and uPA levels in both resected tumor tissue and plasma are of independent prognostic significance for patient survival in several types of human cancer. This system has classically been thought to drive tumor progression by mediating directed extracellular proteolysis on the surface of migrating or invading cells, and intervening with this proteolysis by targeting uPAR has been proposed to represent a novel approach for inhibiting tumor progression. uPAR, also known as PLAUR or CD87, has been implicated in the growth, metastasis, and angiogenesis of several solid and hemotologic malignancies. uPAR is a highly glycosylated, 55-60kDa integral membrane protein linked to the plasma membrane by a glycosylphosphatidylinositol (GPI) anchor. It is part of a cell surface system that also consists of the serine protease uPA and several specific inhibitors (plasminogen activator inhibitors 1 and 2). Additionally, the analysis of CD87 (urokinase-type plasminogen activator receptor - uPAR) expression has a potential role in the diagnostic or prognostic work-up of several hematological malignancies, particularly acute leukemia and multiple myeloma.
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TMPK-00357 | CD229 Protein, Human, Recombinant (His & Avi) | Human | HEK293 | ||
CD229 was strongly and homogeneously overexpressed on the PC of patients with monoclonal gammopathy of undetermined significance (MGUS), smoldering myeloma, MM, and PC leukemia. CD229 was particularly overexpressed on those PC showing an abnormal phenotype such as expression of CD56. Most importantly, CD229 was also highly expressed on those cells in the patients' BM displaying the phenotype of chemotherapy-resistant and myeloma-propagating cells.
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TMPK-01035 | SP17 Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Sperm protein 17 (Sp17) is a highly conserved mammalian protein characterized in rabbit, mouse, monkey, baboon, macaque, human testis and spermatozoa. mRNA encoding Sp17 has been detected in a range of murine and human somatic tissues. It was also recognized in two myeloma cell lines and in neoplastic cells from patients with multiple myeloma and ovarian carcinoma.
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TMPK-00974 | SP17 Protein, Human, Recombinant (His) | Human | E. coli | ||
Sperm protein 17 (Sp17) is a highly conserved mammalian protein characterized in rabbit, mouse, monkey, baboon, macaque, human testis and spermatozoa. mRNA encoding Sp17 has been detected in a range of murine and human somatic tissues. It was also recognized in two myeloma cell lines and in neoplastic cells from patients with multiple myeloma and ovarian carcinoma.
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TMPJ-00331 | IFNAR1 Protein, Rhesus macaque, Recombinant (His) | Rhesus macaque | Human Cells | ||
Interferon‑alpha/beta receptor 1 (IFN‑ alpha / beta R1), also known as IFNAR1, are present in all tissues and even on the surface of most IFN-resistant cells. Isoform 1, isoform 2 and isoform 3 are expressed in the IFN-alpha sensitive myeloma cell line U266B1. Isoform 2 and isoform 3 are expressed in the IFN-alpha resistant myeloma cell line U266R. Isoform 1 is not expressed in IFN-alpha resistant myeloma cell line U266R. It interacts with STAT1 and STAT2, the interaction requires its phosphorylation at Tyr-466. It also interacts with FBXW11, the substrate recognition component of a SCF (SKP1-CUL1-F-box protein) E3 ubiquitin-protein ligase complex.
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TMPK-00358 | CD229 Protein, Human, Recombinant (His & Avi), Biotinylated | Human | HEK293 | ||
CD229 was strongly and homogeneously overexpressed on the PC of patients with monoclonal gammopathy of undetermined significance (MGUS), smoldering myeloma, MM, and PC leukemia. CD229 was particularly overexpressed on those PC showing an abnormal phenotype such as expression of CD56. Most importantly, CD229 was also highly expressed on those cells in the patients' BM displaying the phenotype of chemotherapy-resistant and myeloma-propagating cells.
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TMPY-04409 | GRK6 Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
G protein-coupled receptor kinase 6, also known as G protein-coupled receptor kinase GRK6, GRK6, and GPRK6, is a lipid-anchor protein that belongs to the protein kinase superfamily, AGC Ser/Thr protein kinase family, and GPRK subfamily. GRK6 / GPRK6 contains one AGC-kinase C-terminal domain, one protein kinase domain, and one RGS domain. This protein phosphorylates the activated forms of G protein-coupled receptors thus initiating their deactivation. Several transcript variants encoding different isoforms have been described. GRK6 / GPRK6 is widely expressed. GRK6 / GPRK6 silencing causes suppression of signal transducer and activator of transcription 3 (STAT3) phosphorylation associated with a reduction in MCL1 levels and phosphorylation, illustrating a potent mechanism for the cytotoxicity of GRK6 inhibition in multiple myeloma (MM) tumor cells. GRK6 also appears to be involved in responses to morphine. Inhibition of GRK6 represents a uniquely targeted novel therapeutic strategy in human multiple myeloma.
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TMPK-01193 | GPRC5D Protein-VLP, Mouse, Recombinant | Mouse | HEK293 | ||
Chimeric antigen receptor (CAR) T cells, a type of cell-based immunotherapy, have shown some promising results in multiple myeloma, a bone marrow cancer.The orphan G protein–coupled receptor, class C group 5 member D (GPRC5D), normally expressed only in the hair follicle, Using quantitative immunofluorescence, we determined that GPRC5D protein is expressed on CD138 MM cells from primary marrow samples with a distribution that was similar to, but independent of, BCMA.
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TMPK-00528 | GPRC5D Protein-VLP, Cynomolgus, Recombinant | Cynomolgus | HEK293 | ||
Chimeric antigen receptor (CAR) T cells, a type of cell-based immunotherapy, have shown some promising results in multiple myeloma, a bone marrow cancer.The orphan G protein–coupled receptor, class C group 5 member D (GPRC5D), normally expressed only in the hair follicle, Using quantitative immunofluorescence, we determined that GPRC5D protein is expressed on CD138 MM cells from primary marrow samples with a distribution that was similar to, but independent of, BCMA.
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TMPY-02924 | RGS1 Protein, Human, Recombinant (His) | Human | E. coli | ||
RGS1 (regulator of G-protein signaling 1) has been associated with multiple autoimmune disorders including type I diabetes. RGS1 desensitizes the chemokine receptors CCR7 and CXCR4 that are critical to the localization of T and B cells in lymphoid organs. RGS1 expression may be a prognostic marker for risk stratification and a promising target for the development of a new Multiple myeloma (MM) therapy. The markers in the RGS1 gene might be in linkage disequilibrium with a protective allele that reduces the risk of anxiety and depressive disorders.
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TMPY-06601 | GPRC5D Protein, Human, Recombinant, Biotinylated | Human | HEK293 | ||
Orphan G-protein-coupled receptor family C group 5 member D (GPRC5D) has seven transmembrane segments forming the core of the receptor, as well as an intracellular C-tail and an extracellular N-terminal domain. GPRC5D is highly and selectively expressed on the surface of CD138+ multiple myeloma (MM) cells, whereas in normal tissues, a much lower expression is limited to plasma cells and certain hard keratinizing tissues. This makes GPRC5D a promising marker for monitoring tumor load and a target antigen for MM-specific T cell-engaging therapies such as bispecific antibodies and CAR-T cells.
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TMPY-06719 | GPRC5D Protein, Human, Recombinant (His & FLAG) | Human | HEK293 | ||
Orphan G-protein-coupled receptor family C group 5 member D (GPRC5D) has seven transmembrane segments forming the core of the receptor, as well as an intracellular C-tail and an extracellular N-terminal domain. GPRC5D is highly and selectively expressed on the surface of CD138+ multiple myeloma (MM) cells, whereas in normal tissues, a much lower expression is limited to plasma cells and certain hard keratinizing tissues. This makes GPRC5D a promising marker for monitoring tumor load and a target antigen for MM-specific T cell-engaging therapies such as bispecific antibodies and CAR-T cells.
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TMPY-06806 | GPRC5D Protein, Human, Recombinant (GFP) | Human | HEK293 | ||
Orphan G-protein-coupled receptor family C group 5 member D (GPRC5D) has seven transmembrane segments forming the core of the receptor, as well as an intracellular C-tail and an extracellular N-terminal domain. GPRC5D is highly and selectively expressed on the surface of CD138+ multiple myeloma (MM) cells, whereas in normal tissues, a much lower expression is limited to plasma cells and certain hard keratinizing tissues. This makes GPRC5D a promising marker for monitoring tumor load and a target antigen for MM-specific T cell-engaging therapies such as bispecific antibodies and CAR-T cells.
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TMPY-06718 | GPRC5D Protein, Human, Recombinant (His & FLAG), Detergent | Human | HEK293 | ||
Orphan G-protein-coupled receptor family C group 5 member D (GPRC5D) has seven transmembrane segments forming the core of the receptor, as well as an intracellular C-tail and an extracellular N-terminal domain. GPRC5D is highly and selectively expressed on the surface of CD138+ multiple myeloma (MM) cells, whereas in normal tissues, a much lower expression is limited to plasma cells and certain hard keratinizing tissues. This makes GPRC5D a promising marker for monitoring tumor load and a target antigen for MM-specific T cell-engaging therapies such as bispecific antibodies and CAR-T cells.
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TMPY-06494 | GPRC5D Protein-VLP, Human, Recombinant | Human | HEK293 | ||
Orphan G-protein-coupled receptor family C group 5 member D (GPRC5D) has seven transmembrane segments forming the core of the receptor, as well as an intracellular C-tail and an extracellular N-terminal domain. GPRC5D is highly and selectively expressed on the surface of CD138+ multiple myeloma (MM) cells, whereas in normal tissues, a much lower expression is limited to plasma cells and certain hard keratinizing tissues. This makes GPRC5D a promising marker for monitoring tumor load and a target antigen for MM-specific T cell-engaging therapies such as bispecific antibodies and CAR-T cells.
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TMPY-06807 | GPRC5D Protein, Mouse, Recombinant (Flag) | Mouse | HEK293 | ||
Orphan G-protein-coupled receptor family C group 5 member D (GPRC5D) has seven transmembrane segments forming the core of the receptor, as well as an intracellular C-tail and an extracellular N-terminal domain. GPRC5D is highly and selectively expressed on the surface of CD138+ multiple myeloma (MM) cells, whereas in normal tissues, a much lower expression is limited to plasma cells and certain hard keratinizing tissues. This makes GPRC5D a promising marker for monitoring tumor load and a target antigen for MM-specific T cell-engaging therapies such as bispecific antibodies and CAR-T cells.
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TMPJ-00291 | IL-6R alpha/CD126 Protein, Human, Recombinant (Avi & His), Biotinylated | Human | Human Cells | ||
Interleukin 6 is a potent pleiotropic cytokine that regulates cell growth and differentiation and plays an important role in the immune response. IL6Ra is a part of the receptor for interleukin 6 cytokine. IL6Ra binds to IL6 with low affinity, but does not transduce a signal. Signal activation necessitates an association with IL6ST. Activation may lead to the regulation of the immune response, acute-phase reactions and hematopoiesis. Low concentration of a soluble form of IL6 receptor acts as an agonist of IL6 activity. Dysregulated production of IL6 and this receptor are implicated in the pathogenesis of many diseases, such as multiple myeloma, autoimmune diseases and prostate cancer.
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TMPY-04731 | LAG-3 Protein, Human, Recombinant (mFc) | Human | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-05746 | LAG-3 Protein, Mouse, Recombinant | Mouse | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-04612 | LAG-3 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-06931 | LAG-3 Protein, Human, Recombinant (hFc & Avi), Biotinylated | Human | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-03759 | LAG-3 Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-04611 | LAG-3 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-05130 | LAG-3 Protein, Human, Recombinant, Biotinylated | Human | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPY-04528 | LAG-3 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
LAG3 (Lymphocyte Activating 3) is a Protein Coding gene. 2 alternatively spliced human isoforms have been reported. LAG3, also known as CD223 and Lymphocyte activation gene 3, belongs to the immunoglobulin (Ig) superfamily. The LAG3 gene contains 8 exons. It is selectively expressed in activated T and NK cells. LAG3 contains 4 extracellular Ig-like domains and has a negative regulatory function in T cells. It also acts as a new marker of T cell-induced B cell activation. As a soluble molecule, LAG3 activates antigen-presenting cells through MHC class II signaling, leading to increased antigen-specific T-cell responses in vivo. Diseases associated with LAG3 include Smoldering Myeloma and Kyphoscoliotic Heart Disease.Cancer ImmunotherapyCo-inhibitory Immune Checkpoint TargetsImmune CheckpointImmune Checkpoint TargetsImmunotherapyTargeted Therapy
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TMPJ-00130 | SLAMF2 Protein, Human, Recombinant (hFc & His) | Human | Human Cells | ||
CD48 antigen, also known as B-lymphocyte activation marker BLAST-1, BCM1 surface antigen, Leukocyte antigen MEM-102, TCT.1, CD48, BCM1,and BLAST1, CD48 contains one Ig-like C2-type domain and one Ig-like V-type domain, but does not have a transmembrane domain, however, but is held at the cell surface by a GPI anchor via a C-terminal domain which maybe cleaved to yield a soluble form of the receptor. CD48 may facilitate interaction between activated lymphocytes and be involved in regulating T-cell activation. CD48 plays a vital role as an environmental sensor for regulating progenitor cell numbers and inhibiting tumor development. It is suggested that the anti-CD48 mAb has the potential to become an effective therapeutic mAb against multiple myeloma.
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TMPJ-00694 | BRD4 Protein, Human, Recombinant (His & Flag) | Human | E. coli | ||
Bromodomain-containing protein 4 (BRD4) is a member of the BET class chromatin reader proteins that bind acetylated histones and play a key role in transcriptional regulation and transmission of epigenetic memory. Remains associated with acetylated chromatin throughout the entire cell cycle and provides epigenetic memory for postmitotic G1 gene transcription by preserving acetylated chromatin status and maintaining high-order chromatin structure. BRD bromodomains serve as recognition motifs for acetylated lysine residues on histones, while the NET domain may function by promoting phosphorylation of the C-terminal domain (CTD) of RNA Polymerase II. Some specific inhibitors of BRD4 that prevent binding to acetylated histones by binding Asn-140 and Asn-433 are promising therapeutic molecules for the treatment of leukemias. BRD4 is a potential therapeutic target in many diseases including breast cancer, AML, multiple myeloma, colon cancer and others.
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TMPY-02843 | GPX7 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
GPX7 gene contains 3 distinct gt-ag introns. Transcription produces 4 different mRNAs, 3 alternatively spliced variants, and 1 unspliced form. There are 5 validated alternative polyadenylation sites. The mRNAs appear to differ by overlapping exons with different boundaries. GPX7 is an enzyme. It has molecular functions (glutathione peroxidase activity, oxidoreductase activity) and to localize in various compartments (extracellular space, extracellular region). GPX7 gene has been proposed to participate in pathways (Arachidonic acid metabolism, Glutathione metabolism), and processes (oxidation-reduction, response to oxidative stress). GPX7 modulates the bone turnover after ovariectomy in rats, it does not compensate for the action of estrogen after ovariectomy in rats. It has been shown that three mAbs (GPX7, GPX22, and GPZ35) inhibit IL-6-mediated biological responses such as Ig production in a human B cell line and proliferative responses of a human Lennert's lymphoma-derived T cell line, a human myeloma cell line, and a mouse pro-B cell line-derived transfectant expressing human gp130.
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TMPY-00966 | BCMA/TNFRSF17 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-05595 | BCMA/TNFRSF17 Protein, Mouse, Recombinant (hFc & Avi), Biotinylated | Mouse | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-06757 | BCMA/TNFRSF17 Protein, Human, Recombinant (hFc & Avi), Biotinylated | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-05567 | BCMA/TNFRSF17 Protein, Human (His & hFc), FITC conjugated | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-01211 | BCMA/TNFRSF17 Protein, Mouse, Recombinant (His & hFc) | Mouse | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-05197 | BCMA/TNFRSF17 Protein, Human, Recombinant (mFc) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-02913 | BCMA/TNFRSF17 Protein, Rat, Recombinant (hFc) | Rat | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-05385 | BCMA/TNFRSF17 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-05328 | BCMA/TNFRSF17 Protein, Human, Recombinant (His & Avi) | Human | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-05136 | BCMA/TNFRSF17 Protein, Rhesus, Recombinant, Biotinylated | Rhesus | HEK293 | ||
Tumor necrosis factor receptor superfamily, member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA) or CD269 antigen, is a member of the TNF-receptor superfamily. This receptor is preferentially expressed in mature B lymphocytes, and may be important for B cell development and autoimmune response. This receptor has been shown to specifically bind to the tumor necrosis factor (ligand) superfamily, member 13b (TNFSF13BBAFF), and to lead to NF-kappaB and MAPK8/JNK activation. TNFRSF17/BCMA/CD269 also binds to various TRAF family members, and thus may transduce signals for cell survival and proliferation. TNFRSF17/BCMA/CD269 is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway. The identification of TNFRSF17 as a NF-kappaB-activating receptor for TALL-1 suggests molecular targets for drug development against certain immunodeficient or autoimmune diseases. TNFRSF17/BCMA is a target of donor B-cell immunity in patients with myeloma who respond to DLI. Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.
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TMPY-01017 | uPAR/PLAUR Protein, Mouse, Recombinant (His & hFc) | Mouse | HEK293 | ||
Urokinase plasminogen activator (uPA) and/or its receptor (uPAR) are essential for metastasis, and overexpression of these molecules is strongly correlated with poor prognosis in a variety of malignant tumours. uPAR and uPA levels in both resected tumor tissue and plasma are of independent prognostic significance for patient survival in several types of human cancer. This system has classically been thought to drive tumor progression by mediating directed extracellular proteolysis on the surface of migrating or invading cells, and intervening with this proteolysis by targeting uPAR has been proposed to represent a novel approach for inhibiting tumor progression. uPAR, also known as PLAUR or CD87, has been implicated in the growth, metastasis, and angiogenesis of several solid and hemotologic malignancies. uPAR is a highly glycosylated, 55-60kDa integral membrane protein linked to the plasma membrane by a glycosylphosphatidylinositol (GPI) anchor. It is part of a cell surface system that also consists of the serine protease uPA and several specific inhibitors (plasminogen activator inhibitors 1 and 2). Additionally, the analysis of CD87 (urokinase-type plasminogen activator receptor - uPAR) expression has a potential role in the diagnostic or prognostic work-up of several hematological malignancies, particularly acute leukemia and multiple myeloma.
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TMPY-01710 | IkB alpha/NFKBIA Protein, Human, Recombinant (His) | Human | E. coli | ||
Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkB alpha, NFKBIA, or IKBA), is a member of the NF-kappa-B inhibitor family that function to inhibit the NF-kB transcription factor. NFKBIA inhibits NF-kB by masking the nuclear localization signals (NLS) of NF-kB proteins and keeping them sequestered in an inactive state in the cytoplasm. Also, NFKBIA blocks the ability of NF-κB transcription factors to bind to DNA, which is required for NF-kB's proper functioning. Signal-induced degradation of I kappa B alpha exposes the nuclear localization signal of NF-kappa B, thus allowing it to translocate into the nucleus and activate transcription from responsive genes. An autoregulatory loop is established when NF-kappa B induces expression of the I kappa B alpha gene and newly synthesized I kappa B alpha accumulates in the nucleus where it negatively regulates NF-kappa B-dependent transcription. As part of this post-induction repression, the nuclear export signal on I kappa B alpha mediates the transport of NF-kappa B-I kappa B alpha complexes from the nucleus to the cytoplasm. Deletion of NFKBIA has an effect that is similar to the effect of EGFR amplification in the pathogenesis of glioblastoma and is associated with comparatively short survival. Polymorphisms in NFKBIA may be important in pre-disposition to and outcome after treatment, of multiple myeloma (MM). The NFKBIA gene product, IkappaBalpha, binds to NF-kappaB preventing its activation and is important in mediating resistance to apoptosis in B-cell lymphoproliferative diseases.
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TMPH-03208 | IL-6 Protein, Rabbit, Recombinant (His) | Rabbit | Yeast | ||
Cytokine with a wide variety of biological functions in immunity, tissue regeneration, and metabolism. Binds to IL6R, then the complex associates to the signaling subunit IL6ST/gp130 to trigger the intracellular IL6-signaling pathway. The interaction with the membrane-bound IL6R and IL6ST stimulates 'classic signaling', whereas the binding of IL6 and soluble IL6R to IL6ST stimulates 'trans-signaling'. Alternatively, 'cluster signaling' occurs when membrane-bound IL6:IL6R complexes on transmitter cells activate IL6ST receptors on neighboring receiver cells.; IL6 is a potent inducer of the acute phase response. Rapid production of IL6 contributes to host defense during infection and tissue injury, but excessive IL6 synthesis is involved in disease pathology. In the innate immune response, is synthesized by myeloid cells, such as macrophages and dendritic cells, upon recognition of pathogens through toll-like receptors (TLRs) at the site of infection or tissue injury. In the adaptive immune response, is required for the differentiation of B cells into immunoglobulin-secreting cells. Plays a major role in the differentiation of CD4(+) T cell subsets. Essential factor for the development of T follicular helper (Tfh) cells that are required for the induction of germinal-center formation. Required to drive naive CD4(+) T cells to the Th17 lineage. Also required for proliferation of myeloma cells and the survival of plasmablast cells.; Acts as an essential factor in bone homeostasis and on vessels directly or indirectly by induction of VEGF, resulting in increased angiogenesis activity and vascular permeability. Induces, through 'trans-signaling' and synergistically with IL1B and TNF, the production of VEGF. Involved in metabolic controls, is discharged into the bloodstream after muscle contraction increasing lipolysis and improving insulin resistance. 'Trans-signaling' in central nervous system also regulates energy and glucose homeostasis. Mediates, through GLP-1, crosstalk between insulin-sensitive tissues, intestinal L cells and pancreatic islets to adapt to changes in insulin demand. Also acts as a myokine. Plays a protective role during liver injury, being required for maintenance of tissue regeneration. Also has a pivotal role in iron metabolism by regulating HAMP/hepcidin expression upon inflammation or bacterial infection. Through activation of IL6ST-YAP-NOTCH pathway, induces inflammation-induced epithelial regeneration.
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TMPH-03500 | IL-6 Protein, Sheep, Recombinant (GST) | Sheep | E. coli | ||
Cytokine with a wide variety of biological functions in immunity, tissue regeneration, and metabolism. Binds to IL6R, then the complex associates to the signaling subunit IL6ST/gp130 to trigger the intracellular IL6-signaling pathway. The interaction with the membrane-bound IL6R and IL6ST stimulates 'classic signaling', whereas the binding of IL6 and soluble IL6R to IL6ST stimulates 'trans-signaling'. Alternatively, 'cluster signaling' occurs when membrane-bound IL6:IL6R complexes on transmitter cells activate IL6ST receptors on neighboring receiver cells.; IL6 is a potent inducer of the acute phase response. Rapid production of IL6 contributes to host defense during infection and tissue injury, but excessive IL6 synthesis is involved in disease pathology. In the innate immune response, is synthesized by myeloid cells, such as macrophages and dendritic cells, upon recognition of pathogens through toll-like receptors (TLRs) at the site of infection or tissue injury. In the adaptive immune response, is required for the differentiation of B cells into immunoglobulin-secreting cells. Plays a major role in the differentiation of CD4(+) T cell subsets. Essential factor for the development of T follicular helper (Tfh) cells that are required for the induction of germinal-center formation. Required to drive naive CD4(+) T cells to the Th17 lineage. Also required for proliferation of myeloma cells and the survival of plasmablast cells.; Acts as an essential factor in bone homeostasis and on vessels directly or indirectly by induction of VEGF, resulting in increased angiogenesis activity and vascular permeability. Induces, through 'trans-signaling' and synergistically with IL1B and TNF, the production of VEGF. Involved in metabolic controls, is discharged into the bloodstream after muscle contraction increasing lipolysis and improving insulin resistance. 'Trans-signaling' in central nervous system also regulates energy and glucose homeostasis. Mediates, through GLP-1, crosstalk between insulin-sensitive tissues, intestinal L cells and pancreatic islets to adapt to changes in insulin demand. Also acts as a myokine. Plays a protective role during liver injury, being required for maintenance of tissue regeneration. Also has a pivotal role in iron metabolism by regulating HAMP/hepcidin expression upon inflammation or bacterial infection. Through activation of IL6ST-YAP-NOTCH pathway, induces inflammation-induced epithelial regeneration.
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