目录号 | 产品详情 | 靶点 | |
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T36995 | |||
Potent TBK1 (TANK-binding kinase-1) inhibitor (IC50 = 6 nM). Inhibits the formation of autophagosomes in lung cancer cells. Newman et al (2012) TBK1 kinase addiction in lung cancer cells is mediated via autophagy of Tax1bp1/Ndp52 and non-canonical NF-κB signalling. PLoS ONE 7 e50672 PMID:23209807 |McIver et al (2012) Synthesis and structure-activity relationships of a novel series of pyrimidines as potent inhibitors of TBK1/IKKe kinases. Bioorg.Med.Chem.Lett. 22 7169 PMID:23099093 | |||
T37458 | |||
C18 Phytoceramide (t18:0/18:0) (Cer(t18:0/18:0)) is a bioactive sphingolipid found in S. cerevisiae, wheat grains, and the stratum corneum layer of mammalian epidermis. Cer(t18:0/18:0) is composed of a phytosphingosine backbone amine-linked to a C18 fatty acid chain. Cer(t18:0/18:0) has a role in regulation of apoptosis, cell differentiation, proliferation of smooth muscle cells, and inhibition of the mitochondrial respiratory chain. It also inhibits expression of the allergic cytokines IL-4, TNF-α, and transcription factors c-Jun and NF-κB in histone-stimulated murine skin tissue. Formulations containing cer(t18:0/18:0) have been used used in cosmetics as a skin protectants as they reduce water loss to prevent epidermal dehydration and irritation. | |||
TP2177 | Others | ||
Amyloid precursor c-terminal peptide has the amino acid sequence Gly-Tyr-Glu-Asn-Pro-Thr-Tyr-Lys-Phe-Phe-Glu-Gln-Met-Gln-Asn. APP is best known as the precursor molecule whose proteolysis generates beta-amyloid (Aβ), a 37 to 49 amino acid peptide whose am | |||
T83895 | |||
NCI 126224 是一种 toll-like receptor 4 (TLR4) 的拮抗剂。它在 RAW 264.7 巨噬细胞中,选择性抑制由 TLR4 激动剂 LPS 引起的一氧化氮 (NO) 产生(IC50 = 0.31 µM),而对 TLR7/8 激动剂 R-848、TLR1/2 激动剂 Pam3CSK4 以及 TLR3 激动剂 poly(I:C) 的影响较小;但对于相同细胞中由 TLR2/6 激动剂 FSL-1 引起的 NO 产生,其抑制作用在 0.6 µM 时亦显现。此外,NCI 126224 在 BV-2 微胶质细胞的报告实验中抑制了 LPS 引起的 NF-κB 活性,并在 RAW 264.7 巨噬细胞中降低了 LPS 引起的 IL-1β 和 TNF-α 水平(IC50s = 5.92, 0.42, 和 1.54 µM,分别)。 | |||
T3997 | RIP kinase | ||
WEHI-345 是一种选择性RIPK2 激酶抑制剂,IC50值为 0.13 μM。它在寡聚化结构域刺激下可延迟RIPK2的泛素化和NF-κB 的活化。 | |||
T36713 | |||
Streptochlorin is a bacterial metabolite originally isolated from Streptomyces sp. SF2583 that has diverse biological activities, including antiangiogenic, antiproliferative, and anti-allergic properties. It inhibits TNF-α-induced NF-κB transcriptional activity and decreases proliferation of human umbilical vein endothelial cells (HUVECs) when used at concentrations ranging from 5 to 20 μM. Streptochlorin (12 μg/ml) decreases viability of, as well as induces apoptosis and increases the production of reactive oxygen species (ROS) in, Hep3B human hepatocellular carcinoma cells. It does not induce cytotoxicity in RBL-2H3 mast cells at concentrations up to 100 μM. Streptochlorin prevents degranulation in antigen-stimulated mast cells, as well as inhibits Syk kinase and the Src family kinases LYN and Fyn and reduces the secretion of TNF-α and IL-4 induced by dinitrophenyl-human serum album (DNP-HSA) in RBL-2H3 mast cells. It also decreases swelling and reduces scratching behavior in a mouse model of allergic dermatitis induced by dinitrofluorobenzene (DNFB). | |||
T71303 | |||
Flufenamic acid-d4 is intended for use as an internal standard for the quantification of flufenamic acid by GC- or LC-MS. Flufenamic acid is a non-steroidal anti-inflammatory drug (NSAID) and COX inhibitor (IC50s = 3 and 9.3 µM for human COX-1 and COX-2, respectively). Flufenamic acid inhibits TNF-α-induced increases in COX-2 levels and NF-κB activation in HT-29 colon cancer cells in a concentration-dependent manner. It inhibits calcium influx induced by fMLP or A23187 in human polymorphonuclear leukocytes (PMN) with IC50 values of 29 and 14 µM, respectively. Flufenamic acid also activates various ion channels, including transient receptor potential canonical 6 (TRPC6) and the large-conductance calcium-activated potassium channel (KCa1.1). It also inhibits various ion channels, including TRPC3 and the cystic fibrosis transmembrane conductance regulator (CFTR). Flufenamic acid (20 mg/kg) reduces increases in intestinal fluid secretion and intestinal barrier disruption in mice ...... | |||
T35672 | |||
SMU127 is an agonist of the toll-like receptor 1/2 (TLR1/2) heterodimer.1It induces NF-κB signaling in cells expressing human TLR2 (EC50= 0.55 μM) but not cells expressing human TLR3, -4, -5, -7, or -8 when used at concentrations ranging from 0.1 to 100 μM. SMU127 induces the production of TNF-α in isolated human peripheral blood mononuclear cells (PBMCs) when used at concentrations ranging from 0.01 to 1 μM.In vivo, SMU127 (0.1 mg/animal) reduces tumor volume in a 4T1 murine mammary carcinoma model. 1.Chen, Z., Cen, X., Yang, J., et al.Structure-based discovery of a specific TLR1-TLR2 small molecule agonist from the ZINC drug library databaseChem. Commun. (Camb.)54(81)11411-11414(2018) | |||
TMA1890 | NF-κB | ||
Icariside F2 shows modest α-glucosidase inhibitory (4.60±1.74% to 11.97±3.30%) and antioxidant activities. It also displays potent NF-κB inhibitory effects, with the IC50 value of 16.25 ± 2.19 uM. | |||
T37911 | |||
Resveratrol is a potent phenolic antioxidant found in grapes, red wine, and various berries that also has antiproliferative and anti-inflammatory activity. cis-Resveratrol is the double bond isomer of trans-resveratrol, the more often studied and naturally abundant of the two resveratrol isomers. cis-Resveratrol exhibits antioxidant activity in the µM range similar to that observed with trans-resveratrol. It blocks production of reactive oxygen species (ROS) by inhibition of NAD(P)H oxidase and also inhibits production of nitric oxide. At a concentration of 100 µM, cis-resveratrol significantly inhibits the expression of genes related to the Rel/NF-κB/IκB family, adhesion molecules, and acute-phase proteins in LPS and INF-γ-stimulated murine peritoneal macrophages. cis-Resveratrol inhibits uptake of noradrenaline and 5-HT by synaptosomes from rat brain with IC50 values of 79 and 51 µM, respectively. It also inhibits human monoamine oxidase-A (MOA-A) and MOA-B with IC50 values of 25 and 61 µM, respectively, which is similar to, but slightly less effective than, values obtained with trans-resveratrol. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02603 | STAT6 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Signal transducer and activator of transcription 6 (STAT6) is a transcription factor that is activated by interleukin-4 (IL-4)-induced tyrosine phosphorylation and mediates most of the IL-4-induced gene expression. STAT6 plays a central role in exerting interleukin-4 (IL-4) mediated biological responses and is found to induce the expression of BCL2L1/BCL-XL, which is responsible for the anti-apoptotic activity of IL4. Transcriptional activation by STAT6 requires the interaction with coactivators like p300 and the CREB-binding protein (CBP). NF-κB and tyrosine-phosphorylated Stat6 can directly bind each other in vitro and in vivo, which suggests that the direct interaction between Stat6 and NF-κB may provide a basis for synergistic activation of transcription by IL-4 and activators of NF-κB.
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TMPJ-00662 | RANKL/TNFSF11/CD254 Protein, Human, Recombinant (E. coli) | Human | E. coli | ||
CD254, also known as RANKL, TNFSF11, TRANCE, OPGL and ODF, is a type II membrane protein of the tumor necrosis factor (TNF) superfamily, and affects the immune system and control bone regeneration and remodeling. RANKL is the ligand of nuclear factor (NF)-κB (RANK). When RANKL binds to RANK, it will undergo trimerization and then bind to an adaptor molecule TNF receptor-associated factor 6 (TRAF6). This results in the activation of several downstream signaling cascades, including the NFκB, mitogen-activated protein kinases (MAPK), activating protein 1 (AP-1), and nuclear factor of activated T cells (NFATc1), resulting in the formation of multinucleated bone-resorbing osteoclasts. RANKL is widely expressed in skeletal muscle, thymus, liver, colon, small intestine, adrenal gland, osteoblast, mammary gland epithelial cells, prostate and pancreas.
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TMPJ-01466 | Osteoprotegerin Protein, Human, Recombinant (aa 22-401, His) | Human | HEK293 Cells | ||
TNFRSF11B is a secreted protein, containing 2 death domains and 4 TNFR-Cys repeats. TNFRSF11B is a decoy receptor for the receptor activator of nuclear factor kappa B ligand (RANKL). By binding RANKL, TNFRSF11B inhibits nuclear kappa B (NF-κB) which is a central and rapid acting transcription factor for immune-related genes, and a key regulator of inflammation, innate immunity, and cell survival and differentiation. TNFRSF11B levels are influenced by voltage-dependent calcium channelsCav1.2. TNFRSF11B can reduce the production of osteoclasts by inhibiting the differentiation of osteoclast precursors (osteoclasts are related to monocytes/macrophages and are derived from granulocyte/macrophage-forming colony units (CFU-GM)) into osteoclasts and also regulates the resorption of osteoclasts in vitroand in vivo. TNFRSF11B binding to RANKL on osteoblast/stromal cells, blocks the RANKL-RANK ligand interaction between osteoblast/stromal cells and osteoclast precursors. This has the effect of inhibiting the differentiation of the osteoclast precursor into a mature osteoclast.
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TMPK-00351 | RANK/TNFRSF11A Protein, Human, Recombinant (aa 30-212, hFc) | Human | HEK293 Cells | ||
TNFRSF11A, also known as receptor activator of NF-κB (RANK), activates several signaling pathways, such as NF-κB, JNK, ERK, p38α, and Akt/PKB. RANK/TNFRSF11A is a novel and frequent target for de novo methylation in gliomas, which affects apoptotic activity and focus formation thereby contributing to the molecular pathogenesis of gliomas. RANK/TNFRSF11A Protein, Human, Recombinant (aa 30-212, hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 46.85 kDa and the accession number is Q9Y6Q6-1.
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TMPK-00723 | RANK/TNFRSF11A Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 Cells | ||
TNFRSF11A, also known as receptor activator of NF-κB (RANK), activates several signaling pathways, such as NF-κB, JNK, ERK, p38α, and Akt/PKB. RANK/TNFRSF11A is a novel and frequent target for de novo methylation in gliomas, which affects apoptotic activity and focus formation thereby contributing to the molecular pathogenesis of gliomas. RANK/TNFRSF11A Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 47.0 kDa and the accession number is O35305.
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TMPJ-00674 | RANK/TNFRSF11A Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
Receptor activator of NF-κB(RANK,TNFRSF11A) belongs to one member of tumor necrosis factor receptor family.It is a receptor for TNFSF11/RANKL/TRANCE/OPGL. This gene encodes a type 1 membrane protein with a 30 amino acids (aa) signal peptide, 184 aa extracellular region , a 20 aa transmembrane domain and a 391 aa cytoplasmic region. Human and murine RANK share 81% aa identity in their extracellular domains. RANK is ubiquitous highly expressed in trabecular bone, thymus, small intestine, lung, brain and kidney, but weakly expressed in spleen and bone marrow. After binding its ligand RANKL, RANK can activate signaling pathways such as NF-κB, JNK, ERK, p38, and Akt/PKB, through TRAF protein phosphorylation. RANK/TNFRSF11A signaling is largely considered to be growth promoting and apoptosis reducing such as the effects observed in osteoclasts. RANK/TNFRSF11A was also found to be involved in the regulation of interactions between T-cells and dendritic cells.
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TMPK-00820 | AREG Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Amphiregulin (AREG) is a member of the epidermal growth factor (EGF) family and is expressed in a plethora of cancers. Tumour growth and metastasis were decreased by AREG silencing in an orthotopic model of pancreatic cancer. AREG may play a critical role in cell migration, invasion, and EMT by activating the EGFR/ERK/NF‑κB signalling pathway in pancreatic cancer cells.
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TMPY-03983 | CIRBP Protein, Human, Recombinant (His) | Human | E. coli | ||
CIRBP, also known as cold-inducible RNA-binding protein, plays a protective role in the genotoxic stress response by stabilizing transcripts of genes involved in cell survival. CIRBP responds to a wide array of cellular stresses, including short wavelength ultraviolet light (UVC), at the transcriptional and post-translational level. It acts as a translational activator.CIRBP can bind the 3 translated region of specific transcripts to stabilize them and facilitate their transport to ribosomes for translation. CIRBP affects NF-κB signaling as opposed to IL1B mRNA stability directly.
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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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TMPJ-00617 | IL-33 Protein, Rhesus macaque, Recombinant (His) | Rhesus | E. coli | ||
Interleukin-33 (IL-33) belongs to the IL-1 superfamily. IL33 is highly expressed in endothelial venules found in tonsils, Peyer patches and mesenteric lymph nodes, but almost undetectable in placenta. IL33 induces the production of T helper-2 (Th2)-associated cytokines. IL-33 is a cytokine that mediates its biological effects by binding to and signals through IL1RL1/ST2 and IL-1 Receptor Accessory Protein (IL1RAP), activating intracellular molecules in the NF-κB and MAP kinase signaling pathways that drive production of type 2 cytokines from polarized Th2 cells.
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TMPJ-00086 | CT-1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Cardiotrophin-1, also known as CT-1 and CTF1, is a member of the IL-6 superfamily. It is a sreted cytokine that is expressed in heart, skeletal muscle, prostate and ovary, and to lower levels in lung, kidney, pancreas, thymus, testis and small intestine. The protein exerts its cellular effects by interacting with the glycoprotein 130 (gp130)/leukemia inhibitory factor receptor beta (LIFR) heterodimer. In addition, CT-1 activates phosphatidylinositol 3-kinase (PI-3 kinase) in cardiac myocytes and enhances transcription factor NF-κB DNA -binding activities.
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TMPJ-00280 | TNF R1 Protein, Mouse, Recombinant | Mouse | E. coli | ||
Tumor necrosis factor receptor superfamily member 1A (Tnfrsf1a) is a member of the tumor necrosis factor receptor superfamily. Tnfrsf1a is one of the major receptors for the tumor necrosis factor-alpha. It can activate the transcription factor NF-κB, mediate apoptosis, and function as a regulator of inflammation. Antiapoptotic protein BCL2-associated athanogene 4 (BAG4/SODD) and adaptor proteins TRADD and TRAF2 have been shown to interact with this receptor, and thus play regulatory roles in the signal transduction mediated by the receptor. Germline mutations of the extracellular domains of this receptor were found to be associated with the human genetic disorder called tumor necrosis factor associated periodic syndrome (TRAPS) or periodic fever syndrome
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TMPJ-00083 | NCR3 Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
Natural Cytotoxicity Triggering Receptor 3 (NCR3) along with NKp44 and NKp46 constitute a group of receptors termed “Natural Cytotoxicity Receptors”. They play a major role in triggering NK-mediated killing of most tumor cells lines. NKp30 is a type I transmembrane protein having a single extracellular V-like immunoglobulin domain. NKp30 is selectively expressed both in resting and activated human NK cells. In addition, NKp30 is also involved in NK-mediated induction of dendritic cell (DC) maturation. It has been demonstrated that NK cell activation signaling specifically induces lytic activity against several tumor cell types and synthesis of new NF-κB dependent proteins during the initiation of cytotoxicity.
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TMPY-01176 | cIAP1 Protein, Human, Recombinant (Avi) | Human | E. coli | ||
The cellular inhibitor of apoptosis protein-1 (cIAP1) is a member of the Inhibitor of Apoptosis family proteins are (IAP) whose members are characterized by a novel domain of about 70 amino acids termed baculoviral IAP repeats (BIRs). The BIR domains of cIAP1 and cIAP2 bind to caspases, the key effector proteases of apoptosis. The IAP protein family which can enhance cell survival are crucial regulators of programmed cell death. Both cIAP1 and cIAP2 are the E3 ubiquitin protein isopeptide ligases for Smac, taking part in promoting cancer survival through functioning as E3 ubiquitin ligases. Removal of cIAP1 by genetic deletion may result in NF-κB signaling activation that induces TNFα production and in killing sensitive tumor cells through enhanced TNF-R1 death-receptor signaling and caspase 8 activation. The substrate-dependent E3 activity of cIAPs is mediated by their RING domains and is dependent on the specific interactions between cIAPs and Smac. cIAP1 and cIAP2 are also reported to be regulators of NF-kB activation upon TNFαtreatment.
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TMPJ-00072 | IL-18BPd Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 Cells | ||
Interleukin 18 binding protein (IL-18BP) is a physiological inhibitor that acts through binding to the receptor-binding site of IL-18. IL-18 stimulates INF-γ, which then stimulates 18BP production via NF-κB. The interaction between IL-18 and IL-18BP has a significant role in the inflammation process. IL-18 BPs have four isoforms, a, b, c and d, which are spliced by different ways. The IL-18 BP isoforms a and c each contain one immunoglobulin (Ig)-like C2-type domain which is essential to the binding and neutralizing properties of the binding proteins. The IL-18 BP isoforms b and d lack a complete Ig domain. The expression of IL-18 and the IL-18BP are indentified in immune tissues such as the spleen, but also in nonimmune cells including keratinocytes.
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TMPJ-00060 | IL-25/IL17E Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
Interleukin 25 (IL-25) belongs to the Interleukin 17 (IL-17) family of proteins, which is comprised of six members (IL-17, IL-17B through IL-17F). These proteins are secreted and are structurally related by sharing a conserved cysteine-knot fold near the C-terminus, but have considerable sequence divergence at the N-terminus. With the exception of IL-17B, which exists as a non-covalently linked dimer, all IL-17 family members are disulfide-linked dimers. IL-17 family proteins are pro-inflammatory cytokines that induce local cytokine production and are involved in the regulation of immune functions. Human interleukin-17E (IL17E), also referred to as Interleukin-25 (IL25), is a distinct member of the IL17 cytokine family comprised of at least six members sharing a conserved cysteine-knot structure but divergent at the N-terminus. IL25 is a glycoprotein secreted as dimers by innate effector eosinophils and basophils, and present at very low levels in various peripheral tissues. IL25, together with IL17B, are ligands for the cytokine receptor IL17BR, and the cross-linking induces NF-κB activation and production of the proinflammatory chemokine IL-8, as well as ERK, JNK, and p38 activation. Overexpression of IL25 gene in transgenic mice suggested that this cytokine can regulate hematopoietic and immune functions, and additionally is identified as a proinflammatory cytokine favoring Th2-type immune responses possibly by enhancing the maintenance and functions of adaptive Th2 memory cells.
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