目录号 | 产品详情 | 靶点 | |
---|---|---|---|
T11824L | Syk | ||
Lanraplenib monosuccinate inhibits SYK activity in platelets via the glycoprotein VI (GPVI) receptor without prolonging bleeding time (BT) in monkeys or humans. Lanraplenib monosuccinate is a highly selective and orally active SYK inhibitor (IC50=9.5 nM) in development for the treatment of inflammatory diseases. | |||
T11824 | Syk | ||
Lanraplenib succinate inhibits SYK activity in platelets via the glycoprotein VI (GPVI) receptor without prolonging bleeding time (BT) in monkeys or humans. Lanraplenib succinate is a highly selective and orally active SYK inhibitor (IC50=9.5 nM) in development for the treatment of inflammatory diseases. | |||
T11824LL | Syk | ||
Lanraplenib (GS-9876) 是高效的、选择性的、口服具有活力的 SYK 抑制剂 (IC50=9.5 nM) ,能够用于炎症性疾病的研究。它通过糖蛋白 VI (GPVI) 受体抑制血小板中的 SYK 活性,而不会延长猴子或人类的出血时间 (BT)。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
---|---|---|---|---|---|
TMPK-01190 | GPVI Protein, Human, Recombinant (His) | Human | HEK293 | ||
Although platelets are best known for their role in hemostasis, they are also crucial in development, host defense, inflammation, and tissue repair. Many of these roles are regulated by the immune-like receptors glycoprotein VI (GPVI) and C-type lectin receptor 2 (CLEC-2), which signal through an immunoreceptor tyrosine-based activation motif (ITAM). GPVI is activated by collagen in the subendothelial matrix, by fibrin and fibrinogen in the thrombus, and by a remarkable number of other ligands.
|
|||||
TMPK-01302 | GPVI Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 | ||
Although platelets are best known for their role in hemostasis, they are also crucial in development, host defense, inflammation, and tissue repair. Many of these roles are regulated by the immune-like receptors glycoprotein VI (GPVI) and C-type lectin receptor 2 (CLEC-2), which signal through an immunoreceptor tyrosine-based activation motif (ITAM). GPVI is activated by collagen in the subendothelial matrix, by fibrin and fibrinogen in the thrombus, and by a remarkable number of other ligands.
|
|||||
TMPJ-00605 | GPVI Protein, Mouse, Recombinant (His) | Mouse | Human Cells | ||
Glycoprotein VI (GPVI) is a 63 kDa platelet/megakaryocyte-specific type I transmembrane glycoprotein of the immunoglobulin superfamily that is an important collagen receptor and initiator of platelet activation, aggregation and thrombin generation. GPVI is also a secondary receptor required for platelet spreading on laminin. GPVI associates with the Fc receptor gamma -chain via charged aa in the TM domains of GPVI (arginine) and the FcR gamma (aspartic acid). Collagen binding by the GPVI Ig-like domains initiates signaling through the FcR gamma ITAM sequence. Dimerization of GPVI (2:2 with FcR gamma ) and N-glycosylation greatly enhances collagen binding. Type I and III collagens are strong thrombus-forming components in the vascular subendothelium and atherosclerotic plaques. GPVI initiates binding to fibrillar collagens under flow conditions, then activates integrin alpha 2 beta 1 which binds collagen more tightly. GPVI deficiencies cause only a mild bleeding tendency, probably because integrin alpha 2 beta 1 is able to minimally initiate collagen binding. Normal human GPVI concentration can vary widely and affect maximum thrombin generation. Engagement of GPVI by collagens or other agonists, including autoantibodies, causes calmodulin-regulated metalloproteinase cleavage of the 57 kDa ECD and depletes surface GPVI.
|
|||||
TMPH-01045 | CEACAM1 Protein, Human, Recombinant | Human | E. coli | ||
Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner. Plays a role as coinhibitory receptor in immune response, insulin action and functions also as an activator during angiogenesis. Its coinhibitory receptor function is phosphorylation- and PTPN6 -dependent, which in turn, suppress signal transduction of associated receptors by dephosphorylation of their downstream effectors. Plays a role in immune response, of T cells, natural killer (NK) and neutrophils. Upon TCR/CD3 complex stimulation, inhibits TCR-mediated cytotoxicity by blocking granule exocytosis by mediating homophilic binding to adjacent cells, allowing interaction with and phosphorylation by LCK and interaction with the TCR/CD3 complex which recruits PTPN6 resulting in dephosphorylation of CD247 and ZAP70. Also inhibits T cell proliferation and cytokine production through inhibition of JNK cascade and plays a crucial role in regulating autoimmunity and anti-tumor immunity by inhibiting T cell through its interaction with HAVCR2. Upon natural killer (NK) cells activation, inhibit KLRK1-mediated cytolysis of CEACAM1-bearing tumor cells by trans-homophilic interactions with CEACAM1 on the target cell and lead to cis-interaction between CEACAM1 and KLRK1, allowing PTPN6 recruitment and then VAV1 dephosphorylation. Upon neutrophils activation negatively regulates IL1B production by recruiting PTPN6 to a SYK-TLR4-CEACAM1 complex, that dephosphorylates SYK, reducing the production of reactive oxygen species (ROS) and lysosome disruption, which in turn, reduces the activity of the inflammasome. Downregulates neutrophil production by acting as a coinhibitory receptor for CSF3R by downregulating the CSF3R-STAT3 pathway through recruitment of PTPN6 that dephosphorylates CSF3R. Also regulates insulin action by promoting INS clearance and regulating lipogenesis in liver through regulating insulin signaling. Upon INS stimulation, undergoes phosphorylation by INSR leading to INS clearance by increasing receptor-mediated insulin endocytosis. This inernalization promotes interaction with FASN leading to receptor-mediated insulin degradation and to reduction of FASN activity leading to negative regulation of fatty acid synthesis. INSR-mediated phosphorylation also provokes a down-regulation of cell proliferation through SHC1 interaction resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 and phosphatidylinositol 3-kinase pathways. Functions as activator in angiogenesis by promoting blood vessel remodeling through endothelial cell differentiation and migration and in arteriogenesis by increasing the number of collateral arteries and collateral vessel calibers after ischemia. Also regulates vascular permeability through the VEGFR2 signaling pathway resulting in control of nitric oxide production. Downregulates cell growth in response to EGF through its interaction with SHC1 that mediates interaction with EGFR resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 pathway. Negatively regulates platelet aggregation by decreasing platelet adhesion on type I collagen through the GPVI-FcRgamma complex. Inhibits cell migration and cell scattering through interaction with FLNA; interfers with the interaction of FLNA with RALA. Mediates bile acid transport activity in a phosphorylation dependent manner. Negatively regulates osteoclastogenesis.; Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner. Promotes populations of T cells regulating IgA production and secretion associated with control of the commensal microbiota and resistance to enteropathogens.
|
|||||
TMPH-01044 | CEACAM1 Protein, Human, Recombinant (His & Myc & SUMO) | Human | E. coli | ||
Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner. Plays a role as coinhibitory receptor in immune response, insulin action and functions also as an activator during angiogenesis. Its coinhibitory receptor function is phosphorylation- and PTPN6 -dependent, which in turn, suppress signal transduction of associated receptors by dephosphorylation of their downstream effectors. Plays a role in immune response, of T cells, natural killer (NK) and neutrophils. Upon TCR/CD3 complex stimulation, inhibits TCR-mediated cytotoxicity by blocking granule exocytosis by mediating homophilic binding to adjacent cells, allowing interaction with and phosphorylation by LCK and interaction with the TCR/CD3 complex which recruits PTPN6 resulting in dephosphorylation of CD247 and ZAP70. Also inhibits T cell proliferation and cytokine production through inhibition of JNK cascade and plays a crucial role in regulating autoimmunity and anti-tumor immunity by inhibiting T cell through its interaction with HAVCR2. Upon natural killer (NK) cells activation, inhibit KLRK1-mediated cytolysis of CEACAM1-bearing tumor cells by trans-homophilic interactions with CEACAM1 on the target cell and lead to cis-interaction between CEACAM1 and KLRK1, allowing PTPN6 recruitment and then VAV1 dephosphorylation. Upon neutrophils activation negatively regulates IL1B production by recruiting PTPN6 to a SYK-TLR4-CEACAM1 complex, that dephosphorylates SYK, reducing the production of reactive oxygen species (ROS) and lysosome disruption, which in turn, reduces the activity of the inflammasome. Downregulates neutrophil production by acting as a coinhibitory receptor for CSF3R by downregulating the CSF3R-STAT3 pathway through recruitment of PTPN6 that dephosphorylates CSF3R. Also regulates insulin action by promoting INS clearance and regulating lipogenesis in liver through regulating insulin signaling. Upon INS stimulation, undergoes phosphorylation by INSR leading to INS clearance by increasing receptor-mediated insulin endocytosis. This inernalization promotes interaction with FASN leading to receptor-mediated insulin degradation and to reduction of FASN activity leading to negative regulation of fatty acid synthesis. INSR-mediated phosphorylation also provokes a down-regulation of cell proliferation through SHC1 interaction resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 and phosphatidylinositol 3-kinase pathways. Functions as activator in angiogenesis by promoting blood vessel remodeling through endothelial cell differentiation and migration and in arteriogenesis by increasing the number of collateral arteries and collateral vessel calibers after ischemia. Also regulates vascular permeability through the VEGFR2 signaling pathway resulting in control of nitric oxide production. Downregulates cell growth in response to EGF through its interaction with SHC1 that mediates interaction with EGFR resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 pathway. Negatively regulates platelet aggregation by decreasing platelet adhesion on type I collagen through the GPVI-FcRgamma complex. Inhibits cell migration and cell scattering through interaction with FLNA; interfers with the interaction of FLNA with RALA. Mediates bile acid transport activity in a phosphorylation dependent manner. Negatively regulates osteoclastogenesis.; Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner. Promotes populations of T cells regulating IgA production and secretion associated with control of the commensal microbiota and resistance to enteropathogens.
|