目录号 | 产品详情 | 靶点 | |
---|---|---|---|
TP1770 | |||
CMD178 is an important polypeptide that consistently reduces the expression of Foxp3 and STAT5 by inhibiting the IL-2/s IL-2Rα signaling pathway. | |||
T64110 | |||
Debio 0617B 是一种多激酶抑制剂,能够降低原代人 AML CD34+干/祖细胞的维持和自我更新。Debio 0617B 靶向 STAT3/STAT5 信号上游关键激酶,如 JAK、ABL、SRC 和 III/V 类受体酪氨酸激酶。Debio 0617B 能够用于研究 STAT3 驱动的实体瘤。 | |||
T73330 | |||
JAK-IN-24 是一种 JAK 抑制剂,在 4 μM 或 1 mM ATP 存在时,IC50分别为 0.534 和 24 nM。JAK-IN-24 还抑制 PBMCIL-15诱导的 STAT5磷酸化,IC50为 86.171 nM。 | |||
T77932 | PROTACs | ||
PF15 TFA是一种连接FLT3 kinase配体和CRBN配体的PROTAC,作为FLT3-ITD的高选择性降解剂,DC50值为76.7 nM。该化合物可显著抑制FLT3-ITD阳性细胞增殖,并降低FLT3和STAT5磷酸化水平。PF15 TFA亦能抑制小鼠模型的肿瘤生长,并可用于白血病研究。 | |||
T71654 | |||
APcK110 is a novel Kit inhibitor . APcK110 inhibits proliferation of the mastocytosis cell line HMC1.2 and the SCF-responsive cell line OCI/AML3 in a dose-dependent manner . APcK110 is a more potent inhibitor of OCI/AML3 proliferation than the clinically used Kit inhibitors imatinib and dasatinib and at least as potent as cytarabine. APcK110 inhibits the phosphorylation of Kit, Stat3, Stat5, and Akt in a dose-dependent fashion, showing activity of APcK110 on Kit and its downstream signaling pathways . APcK110 may have potent application in AML. | |||
T14925 | Akt Bcr-Abl STAT | ||
Cenisertib 是一种有效的 ATP 竞争性的多激酶抑制剂,对 Aurora-kinase-A/B,ABL1,AKT,STAT5, FLT3 的活性具有抑制作用,对FER 及其同源物的激酶也显示出抑制作用。Cenisertib 通过抑制肿瘤肥大细胞 (MC) 中几种不同分子靶标的活性抑制其生长,也抑制异种移植模型中胰腺癌,乳腺癌,结肠癌,卵巢癌和肺癌以及白血病的肿瘤生长。 | |||
T74259 | PROTACs | ||
PF15是一种将FLT3 kinase配体与CRBN配体结合的PROTAC,它是FLT3-ITD的高选择性降解剂,显示出76.7 nM的DC50。该化合物能有效抑制FLT3-ITD阳性细胞增殖,并降低FLT3和STAT5的磷酸化水平。在小鼠模型中,PF15也能够抑制肿瘤生长,对白血病研究具有潜在应用价值。 | |||
T83756 | |||
S1H是一种人造肽类模拟物,模仿人类生长激素的第36至51个氨基酸,且为生长激素受体的拮抗剂。在溶液中呈现α-螺旋结构,并在100和200纳摩尔(nM)的浓度下,能降低SK-MEL-28和MALME-3M黑色素瘤细胞系以及IM-9 B细胞淋巴细胞中,由人类生长激素及泌乳素诱导的STAT5磷酸化。 | |||
T74749 | |||
AK-2292 是一种有效和选择性STAT5PROTAC 降解剂,DC50值为 0.10 μM。AK-2292 在体外和体内诱导 STAT5A/B 蛋白的降解。AK-2292 可在急性髓性白血病和慢性髓性白血病异种移植小鼠模型中诱导肿瘤消退。 | |||
T36645 | |||
CAY10763 is a dual inhibitor of indolamine 2,3-dioxygenase 1 (IDO1; IC50= 46 nM) and STAT3 activation.1It binds to STAT3 (Kd= 530 nM) and selectively reduces the levels of STAT3 phosphorylated at the tyrosine in position 705 (STAT3Y705) over phosphorylated STAT3S727, STAT1, and STAT5 in SKOV3 cells when used at a concentration of 500 nM. It also inhibits STAT3 nuclear translocation in SKOV3 cells. CAY10763 is cytotoxic to HCT116, SKOV3, A549, and HepG2 cancer cells (IC50s = 37, 28, 33, and 12 nM, respectively). It reduces tumor growth in B16/F10 mouse melanoma and HepG2 mouse xenograft models when administered at doses of 100 and 10 mg/kg, respectively. 1.Huang, R., Jing, X., Huang, X., et al.Bifunctional naphthoquinone aromatic amide-oxime derivatives exert combined immunotherapeutic and antitumor effects through simultaneous targeting of indoleamine-2,3-dioxygenase and signal transducer and activator of transcription 3J. Med. Chem.63(4)1544-1563(2020) |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
---|---|---|---|---|---|
TMPJ-00166 | SCF Protein, Mouse, Recombinant | Mouse | E. coli | ||
Mouse stem cell factor (SCF), is the ligand for the receptor-type protein-tyrosine kinase KIT. It plays an essential role in the regulation of cell survival and proliferation, hematopoiesis, stem cell maintenance, gametogenesis, mast cell development, migration and function, and in melanogenesis. KITLG/SCF binding can activate several signaling pathways. It also promotes phosphorylation of PIK3R1, which is the regulatory subunit of phosphatidylinositol 3-kinase, and subsequent activation of the kinase AKT1. KITLG/SCF and KIT also transmit signals via GRB2 and activation of RAS, RAF1 and the MAP kinases MAPK1/ERK2 and/or MAPK3/ERK1. KITLG/SCF and KIT promote activation of STAT family members STAT1, STAT3 and STAT5.
|
|||||
TMPY-02333 | ULBP-2 Protein, Human, Recombinant (His) | Human | HEK293 | ||
NKG2D ligand 2, also known as N2DL-2, NKG2DL2, ALCAN-alpha, Retinoic acid early transcript 1H, UL16-binding protein 2, ULBP2 and N2DL2, is cell membrane protein that belongs to the MHC class I family. ULBP2 / N2DL-2 is expressed in various types of cancer cell lines and in the fetus, but not in normal tissues. ULBP2 / N2DL-2 is a ligand for the NKG2D receptor, together with at least ULBP1 and ULBP3. ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway.
|
|||||
TMPY-05592 | ULBP-2 Protein, Human, Recombinant(aa 1-217, His&AVI),Biotinylated | Human | HEK293 | ||
NKG2D ligand 2, also known as N2DL-2, NKG2DL2, ALCAN-alpha, Retinoic acid early transcript 1H, UL16-binding protein 2, ULBP2 and N2DL2, is cell membrane protein that belongs to the MHC class I family. ULBP2 / N2DL-2 is expressed in various types of cancer cell lines and in the fetus, but not in normal tissues. ULBP2 / N2DL-2 is a ligand for the NKG2D receptor, together with at least ULBP1 and ULBP3. ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway.
|
|||||
TMPY-04632 | IL-15 Protein, Human, Recombinant | Human | E. coli | ||
The protein encoded by the IL15 gene is a cytokine that regulates T and natural killer cell activation and proliferation. This cytokine and interleukine 2 share many biological activities. They are found to bind common hematopoietic receptor subunits and may compete for the same receptor, and thus negatively regulate each other's activity. The number of CD8+ memory cells is shown to be controlled by a balance between this cytokine and IL2. This cytokine induces the activation of JAK kinases, as well as the phosphorylation and activation of transcription activators STAT3, STAT5, and STAT6. Studies of the mouse counterpart suggested that this cytokine may increase the expression of apoptosis inhibitor BCL2L1/BCL-x(L), possibly through the transcription activation activity of STAT6, and thus prevent apoptosis. Alternatively, spliced transcript variants of this gene have been reported.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
|
|||||
TMPY-01870 | IL-9 Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
Interleukin 9, also known as IL-9, is a cytokine (cell signaling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-β1 to differentiate naive CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and the absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.
|
|||||
TMPK-00136 | ULBP-2 Protein, Human, Recombinant (His & Avi) | Human | HEK293 | ||
ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway, mediating natural killer cell cytotoxicity.
|
|||||
TMPJ-01003 | STAT5B Protein, Human, Recombinant (His) | Human | E. coli | ||
Signal Transducer and Activator of Transcription 5b (STAT5B) is a member of the STAT family of transcription factors. They are responsible for an array of cellular activities including regulating growth, survival, differentiation, motility, and the immune response. STAT5B mediates the signal transduction triggered by various cell ligands, such as IL2, IL4, CSF1, and different growth hormones. It has been shown to be involved in diverse biological processes, such as TCR signaling, apoptosis, adult mammary gland development, and sexual dimorphism of liver gene expression. Signal transduction and activator of transcription 5 (STAT5) is a member of the Jak/STAT signal transduction pathway and is activated by a variety of cytokines (IL22, IL6). STAT5 has two isoforms (A and B) that share 93% amino acid identity and bind the DNA consensus site TTCN3GAA. STAT5 mediates cytokine signaling by acting as a signal transducer in the cytoplasm and, upon phosphorylation, translocates to the nucleus and activates transcription of specific genes. STAT5 is involved in a wide array of biological processes ranging from regulating apoptosis to adult mammary gland proliferation, differentiation and survival.
|
|||||
TMPH-03204 | GHR Protein, Rabbit, Recombinant (His & Myc) | Rabbit | in vitro E. coli expression system | ||
Receptor for pituitary gland growth hormone involved in regulating postnatal body growth. On ligand binding, couples to, and activates the JAK2/STAT5 pathway.; The soluble form (GHBP) acts as a reservoir of growth hormone in plasma and may be a modulator/inhibitor of GH signaling.
|
|||||
TMPH-03287 | EPOR Protein, Rat, Recombinant (His & SUMO) | Rat | E. coli | ||
Receptor for erythropoietin. Mediates erythropoietin-induced erythroblast proliferation and differentiation. Upon EPO stimulation, EPOR dimerizes triggering the JAK2/STAT5 signaling cascade. In some cell types, can also activate STAT1 and STAT3. May also activate LYN tyrosine kinase.
|
|||||
TMPH-02440 | GHR Protein, Rhesus macaque, Recombinant (His) | Rhesus | E. coli | ||
Receptor for pituitary gland growth hormone involved in regulating postnatal body growth. On ligand binding, couples to, and activates the JAK2/STAT5 pathway.; The soluble form (GHBP) acts as a reservoir of growth hormone in plasma and may be a modulator/inhibitor of GH signaling.
|
|||||
TMPH-03112 | GHR Protein, Pig, Recombinant (His) | Sus scrofa (Pig) | E. coli | ||
Receptor for pituitary gland growth hormone involved in regulating postnatal body growth. On ligand binding, couples to, and activates the JAK2/STAT5 pathway.; The soluble form (GHBP) acts as a reservoir of growth hormone in plasma and may be a modulator/inhibitor of GH signaling.
|
|||||
TMPK-00025 | IL-9 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
IL-9 is a pleiotropic cytokine that influences various distinct functions of different target cells such as T cells, B cells, mast cells and airway epithelial cells by activating STAT1, STAT3 and STAT5. Because of its pleiotropic functions, IL-9 has been demonstrated to be involved in several diseases, such as cancer, autoimmunity and other pathogen-mediated immune-regulated diseases. In this review, we focus on the role of Th9 and IL-9-producing cells in allergic asthma.
|
|||||
TMPH-02274 | JAK2 Protein, Human, Recombinant (His) | Human | E. coli | ||
Non-receptor tyrosine kinase involved in various processes such as cell growth, development, differentiation or histone modifications. Mediates essential signaling events in both innate and adaptive immunity. In the cytoplasm, plays a pivotal role in signal transduction via its association with type I receptors such as growth hormone (GHR), prolactin (PRLR), leptin (LEPR), erythropoietin (EPOR), thrombopoietin (THPO); or type II receptors including IFN-alpha, IFN-beta, IFN-gamma and multiple interleukins. Following ligand-binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins. Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor. Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription. For example, cell stimulation with erythropoietin (EPO) during erythropoiesis leads to JAK2 autophosphorylation, activation, and its association with erythropoietin receptor (EPOR) that becomes phosphorylated in its cytoplasmic domain. Then, STAT5 (STAT5A or STAT5B) is recruited, phosphorylated and activated by JAK2. Once activated, dimerized STAT5 translocates into the nucleus and promotes the transcription of several essential genes involved in the modulation of erythropoiesis. Part of a signaling cascade that is activated by increased cellular retinol and that leads to the activation of STAT5 (STAT5A or STAT5B). In addition, JAK2 mediates angiotensin-2-induced ARHGEF1 phosphorylation. Plays a role in cell cycle by phosphorylating CDKN1B. Cooperates with TEC through reciprocal phosphorylation to mediate cytokine-driven activation of FOS transcription. In the nucleus, plays a key role in chromatin by specifically mediating phosphorylation of 'Tyr-41' of histone H3 (H3Y41ph), a specific tag that promotes exclusion of CBX5 (HP1 alpha) from chromatin.
|
|||||
TMPK-00568 | IL-9 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 | ||
IL-9 is a pleiotropic cytokine that influences various distinct functions of different target cells such as T cells, B cells, mast cells and airway epithelial cells by activating STAT1, STAT3 and STAT5. Because of its pleiotropic functions, IL-9 has been demonstrated to be involved in several diseases, such as cancer, autoimmunity and other pathogen-mediated immune-regulated diseases. In this review, we focus on the role of Th9 and IL-9-producing cells in allergic asthma.
|
|||||
TMPJ-00894 | SCF Protein, Rat, Recombinant (His) | Rat | E. coli | ||
Stem cell factor (SCF), is the ligand for the receptor-type protein-tyrosine kinase KIT. It plays an essential role in the regulation of cell survival and proliferation, hematopoiesis, stem cell maintenance, gametogenesis, mast cell development, migration and function, and in melanogenesis. KITLG/SCF binding can activate several signaling pathways. It also promotes phosphorylation of PIK3R1, which is the regulatory subunit of phosphatidylinositol 3-kinase, and subsequent activation of the kinase AKT1. KITLG/SCF and KIT also transmit signals via GRB2 and activation of RAS, RAF1 and the MAP kinases MAPK1/ERK2 and/or MAPK3/ERK1. KITLG/SCF and KIT promote activation of STAT family members STAT1, STAT3 and STAT5.
|
|||||
TMPY-02334 | ULBP-2 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
NKG2D ligand 2, also known as N2DL-2, NKG2DL2, ALCAN-alpha, Retinoic acid early transcript 1H, UL16-binding protein 2, ULBP2 and N2DL2, is cell membrane protein that belongs to the MHC class I family. ULBP2 / N2DL-2 is expressed in various types of cancer cell lines and in the fetus, but not in normal tissues. ULBP2 / N2DL-2 is a ligand for the NKG2D receptor, together with at least ULBP1 and ULBP3. ULBPs activate multiple signaling pathways in primary NK cells, resulting in the production of cytokines and chemokines. Binding of ULBPs ligands to NKG2D induces calcium mobilization and activation of the JAK2, STAT5, ERK and PI3K kinase/Akt signal transduction pathway.
|
|||||
TMPK-00026 | IL-9 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
IL-9 is a pleiotropic cytokine that influences various distinct functions of different target cells such as T cells, B cells, mast cells and airway epithelial cells by activating STAT1, STAT3 and STAT5. Because of its pleiotropic functions, IL-9 has been demonstrated to be involved in several diseases, such as cancer, autoimmunity and other pathogen-mediated immune-regulated diseases. In this review, we focus on the role of Th9 and IL-9-producing cells in allergic asthma.
|
|||||
TMPY-04049 | IL-15 Protein, Human, Recombinant (His) | Human | E. coli | ||
The protein encoded by the IL15 gene is a cytokine that regulates T and natural killer cell activation and proliferation. This cytokine and interleukine 2 share many biological activities. They are found to bind common hematopoietic receptor subunits and may compete for the same receptor, and thus negatively regulate each other's activity. The number of CD8+ memory cells is shown to be controlled by a balance between this cytokine and IL2. This cytokine induces the activation of JAK kinases, as well as the phosphorylation and activation of transcription activators STAT3, STAT5, and STAT6. Studies of the mouse counterpart suggested that this cytokine may increase the expression of apoptosis inhibitor BCL2L1/BCL-x(L), possibly through the transcription activation activity of STAT6, and thus prevent apoptosis. Alternatively, spliced transcript variants of this gene have been reported.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
|
|||||
TMPJ-00530 | TSLPR Protein, Mouse, Recombinant (hFc) | Mouse | Human Cells | ||
The cytokine thymic stromal lymphopoietin receptor (TSLPR) is consisting of a common γ receptor–like chain (TSLPR-γ) and a common interleukin 7 (IL-7) Rα chain that belongs to the type 1 cytokine receptor family. Transfection of TSLPR cDNA result in only low affinity binding, while cotransfection of the IL-7Rα chain cDNA shows high affinity binding. TSLP and TSLPR play a critical role in the initiation of allergic diseases in mice. The TSLP R cDNA encodes a transmembrane receptor containing 370 amino acids (aa) with two potential N-linked glycosylation sites and a cytoplasmic domain of 104 aa including a single tyrosine residue. TSLPR can mediate signaling of the signal transducer and activator of transcription 5 (Stat5) by TSLP. TSLP R is broadly expressed in the immune and hematopoietic cells, particularly in hematopoietic progenitors and myeloid cells.
|
|||||
TMPJ-00531 | TSLPR Protein, Mouse, Recombinant (His) | Mouse | Human Cells | ||
The cytokine thymic stromal lymphopoietin receptor (TSLPR) is consisting of a common γ receptor–like chain (TSLPR-γ) and a common interleukin 7 (IL-7) Rα chain that belongs to the type 1 cytokine receptor family. Transfection of TSLPR cDNA result in only low affinity binding, while cotransfection of the IL-7Rα chain cDNA shows high affinity binding. TSLP and TSLPR play a critical role in the initiation of allergic diseases in mice. The TSLP R cDNA encodes a transmembrane receptor containing 370 amino acids (aa) with two potential N-linked glycosylation sites and a cytoplasmic domain of 104 aa including a single tyrosine residue. TSLPR can mediate signaling of the signal transducer and activator of transcription 5 (Stat5) by TSLP. TSLP R is broadly expressed in the immune and hematopoietic cells, particularly in hematopoietic progenitors and myeloid cells.
|
|||||
TMPJ-00346 | PRLR Protein, Mouse, Recombinant (hFc) | Mouse | Human Cells | ||
The prolactin receptor (PRLR) is a member of the class I cytokine/lactogen receptor family which mediates the diverse cellular actions of prolactin in several tissues. PRLRs are expressed in normal and neoplastic human breast tissue, and in most breast cancer cells. PRLR contains an extracellular region that binds prolactin, a transmembrane region, and a cytoplasmatic region required for the activation of the Jak2–Stat5 signal transduction pathway by Prl which is essential for transcriptional activation of all known prolactin regulated genes. PRLRs have also been observed in ovarian follicular cells of mice, pigs, sheep, deer, and humans, as well as in luteal tissue in cow and horse ovaries. Furthermore, PRLR knockout mice exhibit failure of embryonic implantation, reduced number of mature oocytes, and low fertilization rates. Knockout females also display a reduced number of primary follicles.
|
|||||
TMPJ-00347 | PRLR Protein, Mouse, Recombinant (His) | Mouse | Human Cells | ||
The prolactin receptor (PRLR) is a member of the class I cytokine/lactogen receptor family which mediates the diverse cellular actions of prolactin in several tissues. PRLRs are expressed in normal and neoplastic human breast tissue, and in most breast cancer cells. PRLR contains an extracellular region that binds prolactin, a transmembrane region, and a cytoplasmatic region required for the activation of the Jak2–Stat5 signal transduction pathway by Prl which is essential for transcriptional activation of all known prolactin regulated genes. PRLRs have also been observed in ovarian follicular cells of mice, pigs, sheep, deer, and humans, as well as in luteal tissue in cow and horse ovaries. Furthermore, PRLR knockout mice exhibit failure of embryonic implantation, reduced number of mature oocytes, and low fertilization rates. Knockout females also display a reduced number of primary follicles.
|
|||||
TMPY-05221 | IL-9 Protein, Mouse, Recombinant (His) | Mouse | Baculovirus-Insect Cells | ||
Interleukin 9, also known as IL-9, is a cytokine (cell signaling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-β1 to differentiate naive CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and the absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.
|
|||||
TMPY-01448 | GHR/Growth Hormone R Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Growth hormone receptor, also known as GH receptor and GHR, is a single-pass type I membrane protein which belongs to thetype I cytokine receptor family and type 1 subfamily. GHR contains onefibronectin type-III domain. Growth hormone receptor / GHR is expressed in various tissues with high expression in liver and skeletal muscle. Isoform4of GHR is predominantly expressed in kidney, bladder, adrenal gland and brain stem. Isoform1 expression of GHR in placenta is predominant in chorion and decidua. Isoform4is highly expressed in placental villi. Isoform2of GHR is expressed in lung, stomach and muscle. Growth hormone receptor / GHR is a receptor for pituitary gland growth hormone. It is involved in regulating postnatal body growth. On ligand binding, it couples to the JAK2 / STAT5 pathway. Isoform2of GHR up-regulates the production of GHBP and acts as a negative inhibitor of GH signaling. Defects in GHR are a cause of Laron syndrome (LARS) which is a severe form of growth hormone insensitivity characterized by growth impairment, short stature, dysfunctional growth hormone receptor, and failure to generate insulin-like growth factor I in response to growth hormone. Defects in GHR may also be a cause of idiopathic short stature autosomal (ISSA) which is defined by a subnormal rate of growth.
|
|||||
TMPY-04281 | GHR/Growth Hormone R Protein, Rat, Recombinant (hFc) | Rat | HEK293 | ||
Growth hormone receptor, also known as GH receptor and GHR, is a single-pass type I membrane protein which belongs to thetype I cytokine receptor family and type 1 subfamily. GHR contains onefibronectin type-III domain. Growth hormone receptor / GHR is expressed in various tissues with high expression in liver and skeletal muscle. Isoform4of GHR is predominantly expressed in kidney, bladder, adrenal gland and brain stem. Isoform1 expression of GHR in placenta is predominant in chorion and decidua. Isoform4is highly expressed in placental villi. Isoform2of GHR is expressed in lung, stomach and muscle. Growth hormone receptor / GHR is a receptor for pituitary gland growth hormone. It is involved in regulating postnatal body growth. On ligand binding, it couples to the JAK2 / STAT5 pathway. Isoform2of GHR up-regulates the production of GHBP and acts as a negative inhibitor of GH signaling. Defects in GHR are a cause of Laron syndrome (LARS) which is a severe form of growth hormone insensitivity characterized by growth impairment, short stature, dysfunctional growth hormone receptor, and failure to generate insulin-like growth factor I in response to growth hormone. Defects in GHR may also be a cause of idiopathic short stature autosomal (ISSA) which is defined by a subnormal rate of growth.
|
|||||
TMPJ-00047 | IL-31 Protein, Human, Recombinant | Human | E. coli | ||
Human Interleukin 31 (IL-31) is a cytokine containing a four-helix bundle structure. It shares several structural and functional characteristics with IL-6, Oncostatin M, LIF, and Cardiotrophin-1. Human IL-31 cDNA encodes a 164 amino acid precursor that contains a 23 amino acid signal peptide and a 141 amino acid mature protein. Human and mouse IL-31 share 24% sequence identity in the mature region. IL-31 is mainly associated with activated T cells and is preferentially expressed by type 2 helper T cells (Th2). IL-31 signals via a heterodimeric receptor complex composed of a gp130 related molecule termed IL-31RA (also GPL and GLMR) and an Oncostatin M receptor (OSM Rβ). The IL-31 receptor is constitutively expressed by keratinocytes and upregulated by IFNγ on monocytes. GPL/OSMR signaling is a strong activator of STAT3 and STAT5, and can also activate STAT1, Jak1, and Jak2 signaling pathways. IL-31 regulated immune responses have been implicated in skin physiology and inflammatory skin diseases. Studies have shown that IL31 induces severe pruritis (itching) and dermatitis in transgenic mice.
|
|||||
TMPY-02007 | GHR/Growth Hormone R Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
Growth hormone receptor, also known as GH receptor and GHR, is a single-pass type I membrane protein which belongs to thetype I cytokine receptor family and type 1 subfamily. GHR contains onefibronectin type-III domain. Growth hormone receptor / GHR is expressed in various tissues with high expression in liver and skeletal muscle. Isoform4of GHR is predominantly expressed in kidney, bladder, adrenal gland and brain stem. Isoform1 expression of GHR in placenta is predominant in chorion and decidua. Isoform4is highly expressed in placental villi. Isoform2of GHR is expressed in lung, stomach and muscle. Growth hormone receptor / GHR is a receptor for pituitary gland growth hormone. It is involved in regulating postnatal body growth. On ligand binding, it couples to the JAK2 / STAT5 pathway. Isoform2of GHR up-regulates the production of GHBP and acts as a negative inhibitor of GH signaling. Defects in GHR are a cause of Laron syndrome (LARS) which is a severe form of growth hormone insensitivity characterized by growth impairment, short stature, dysfunctional growth hormone receptor, and failure to generate insulin-like growth factor I in response to growth hormone. Defects in GHR may also be a cause of idiopathic short stature autosomal (ISSA) which is defined by a subnormal rate of growth.
|
|||||
TMPY-00459 | IL-9 Protein, Rat, Recombinant (His) | Rat | Baculovirus-Insect Cells | ||
Interleukin 9, also known as IL-9, is a cytokine (cell signaling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-β1 to differentiate naive CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and the absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.
|
|||||
TMPY-00977 | GHR/Growth Hormone R Protein, Mouse, Recombinant (His & hFc) | Mouse | HEK293 | ||
Growth hormone receptor, also known as GH receptor and GHR, is a single-pass type I membrane protein which belongs to thetype I cytokine receptor family and type 1 subfamily. GHR contains onefibronectin type-III domain. Growth hormone receptor / GHR is expressed in various tissues with high expression in liver and skeletal muscle. Isoform4of GHR is predominantly expressed in kidney, bladder, adrenal gland and brain stem. Isoform1 expression of GHR in placenta is predominant in chorion and decidua. Isoform4is highly expressed in placental villi. Isoform2of GHR is expressed in lung, stomach and muscle. Growth hormone receptor / GHR is a receptor for pituitary gland growth hormone. It is involved in regulating postnatal body growth. On ligand binding, it couples to the JAK2 / STAT5 pathway. Isoform2of GHR up-regulates the production of GHBP and acts as a negative inhibitor of GH signaling. Defects in GHR are a cause of Laron syndrome (LARS) which is a severe form of growth hormone insensitivity characterized by growth impairment, short stature, dysfunctional growth hormone receptor, and failure to generate insulin-like growth factor I in response to growth hormone. Defects in GHR may also be a cause of idiopathic short stature autosomal (ISSA) which is defined by a subnormal rate of growth.
|