Esta buscando: JNK-IN-8

Numero del catalogo: (BOSSBS-3353R-CY5.5)

Proveedor: Bioss

Descripción: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B,induces 14-3-3-proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-9458R-A750)

Proveedor: Bioss

Descripción: TNNI3K, also known as CARK, is a 936 amino acid serine/threonine-protein kinase that is highly expressed in heart. Overexpression of TNNI3K leads to improved cardiac function by enhancing beating frequency and increasing contractile force and epinephrine response. TNNI3K suppresses phosphorylation of cardiac troponin I and p38/JNK-mediated apoptosis, therefore protecting the myocardium from ischemic injury. Administration of TNNI3K to mice with myocardial infarction improves cardiac performance and attentuates ventricular remodeling, suggesting that TNNI3K could be a promising target in the treatment of cardiac diseases. There are four isoforms of TNNI3K that are produced as a result of alternative splicing events.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-3353R-A555)

Proveedor: Bioss

Descripción: Proto-oncogene with serine/threonine kinase activity involved in cell survival and cell proliferation and thus providing a selective advantage in tumorigenesis. Exerts its oncogenic activity through: the regulation of MYC transcriptional activity, the regulation of cell cycle progression and by phosphorylation and inhibition of proapoptotic proteins (BAD, MAP3K5, FOXO3). Phosphorylation of MYC leads to an increase of MYC protein stability and thereby an increase of transcriptional activity. The stabilization of MYC exerted by PIM1 might explain partly the strong synergism between these two oncogenes in tumorigenesis. Mediates survival signaling through phosphorylation of BAD, which induces release of the anti-apoptotic protein Bcl-X(L)/BCL2L1. Phosphorylation of MAP3K5, an other proapoptotic protein, by PIM1, significantly decreases MAP3K5 kinase activity and inhibits MAP3K5-mediated phosphorylation of JNK and JNK/p38MAPK subsequently reducing caspase-3 activation and cell apoptosis. Stimulates cell cycle progression at the G1-S and G2-M transitions by phosphorylation of CDC25A and CDC25C. Phosphorylation of CDKN1A, a regulator of cell cycle progression at G1, results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. Promote cell cycle progression and tumorigenesis by down-regulating expression of a regulator of cell cycle progression, CDKN1B, at both transcriptional and post-translational levels. Phosphorylation of CDKN1B,induces 14-3-3-proteins binding, nuclear export and proteasome-dependent degradation. May affect the structure or silencing of chromatin by phosphorylating HP1 gamma/CBX3. Acts also as a regulator of homing and migration of bone marrow cells involving functional interaction with the CXCL12-CXCR4 signaling axis.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-9458R-A647)

Proveedor: Bioss

Descripción: TNNI3K, also known as CARK, is a 936 amino acid serine/threonine-protein kinase that is highly expressed in heart. Overexpression of TNNI3K leads to improved cardiac function by enhancing beating frequency and increasing contractile force and epinephrine response. TNNI3K suppresses phosphorylation of cardiac troponin I and p38/JNK-mediated apoptosis, therefore protecting the myocardium from ischemic injury. Administration of TNNI3K to mice with myocardial infarction improves cardiac performance and attentuates ventricular remodeling, suggesting that TNNI3K could be a promising target in the treatment of cardiac diseases. There are four isoforms of TNNI3K that are produced as a result of alternative splicing events.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-9458R-FITC)

Proveedor: Bioss

Descripción: TNNI3K, also known as CARK, is a 936 amino acid serine/threonine-protein kinase that is highly expressed in heart. Overexpression of TNNI3K leads to improved cardiac function by enhancing beating frequency and increasing contractile force and epinephrine response. TNNI3K suppresses phosphorylation of cardiac troponin I and p38/JNK-mediated apoptosis, therefore protecting the myocardium from ischemic injury. Administration of TNNI3K to mice with myocardial infarction improves cardiac performance and attentuates ventricular remodeling, suggesting that TNNI3K could be a promising target in the treatment of cardiac diseases. There are four isoforms of TNNI3K that are produced as a result of alternative splicing events.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-13654R-A350)

Proveedor: Bioss

Descripción: Several mammalian kinases have been identified with sequence similarity to the Saccharomyces cerevisiae serine/threonine kinase STE20. STE20 is involved in relaying signals from G-protein coupled receptors to cytosolic MAP kinase cascades, and it lies upstream of a MAP kinase kinase kinase. Mammalian STE20-like kinases include KHS, GLK, NIK, YSK1, HPK1, Krs-1, Krs-2 and GC kinase. KHS (for kinase homologous to SPS1/STE20) is a protein that is most closely related to GC kinase. The KHS kinase has been shown to activate a variety of substrates, including JNK, suggesting a role in stress response.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-13654R-A488)

Proveedor: Bioss

Descripción: Several mammalian kinases have been identified with sequence similarity to the Saccharomyces cerevisiae serine/threonine kinase STE20. STE20 is involved in relaying signals from G-protein coupled receptors to cytosolic MAP kinase cascades, and it lies upstream of a MAP kinase kinase kinase. Mammalian STE20-like kinases include KHS, GLK, NIK, YSK1, HPK1, Krs-1, Krs-2 and GC kinase. KHS (for kinase homologous to SPS1/STE20) is a protein that is most closely related to GC kinase. The KHS kinase has been shown to activate a variety of substrates, including JNK, suggesting a role in stress response.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-9001R-HRP)

Proveedor: Bioss

Descripción: Negative regulator of MYD88- and TRIF-dependent toll-like receptor signaling pathway which plays a pivotal role in activating axonal degeneration following injury. Promotes Wallerian degeneration an injury-induced axonal death pathway which involves degeneration of an axon distal to the injury site. Can activate neuronal death in response to stress. Regulates dendritic arborization through the MAPK4-JNK pathway. Involved in innate immune response. Inhibits both TICAM1/TRIF- and MYD88-dependent activation of JUN/AP-1, TRIF-dependent activation of NF-kappa-B and IRF3, and the phosphorylation of MAPK14/p38.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-9001R-A488)

Proveedor: Bioss

Descripción: Negative regulator of MYD88- and TRIF-dependent toll-like receptor signaling pathway which plays a pivotal role in activating axonal degeneration following injury. Promotes Wallerian degeneration an injury-induced axonal death pathway which involves degeneration of an axon distal to the injury site. Can activate neuronal death in response to stress. Regulates dendritic arborization through the MAPK4-JNK pathway. Involved in innate immune response. Inhibits both TICAM1/TRIF- and MYD88-dependent activation of JUN/AP-1, TRIF-dependent activation of NF-kappa-B and IRF3, and the phosphorylation of MAPK14/p38.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-13654R-CY3)

Proveedor: Bioss

Descripción: Several mammalian kinases have been identified with sequence similarity to the Saccharomyces cerevisiae serine/threonine kinase STE20. STE20 is involved in relaying signals from G-protein coupled receptors to cytosolic MAP kinase cascades, and it lies upstream of a MAP kinase kinase kinase. Mammalian STE20-like kinases include KHS, GLK, NIK, YSK1, HPK1, Krs-1, Krs-2 and GC kinase. KHS (for kinase homologous to SPS1/STE20) is a protein that is most closely related to GC kinase. The KHS kinase has been shown to activate a variety of substrates, including JNK, suggesting a role in stress response.

UOM: 1 * 100 µl

Promoción

Numero del catalogo: (BOSSBS-4162R-A750)

Proveedor: Bioss

Descripción: The protein encoded by this gene is a member of the PP2C family of Ser/Thr protein phosphatases. PP2C family members are known to be negative regulators of cell stress response pathways. This phosphatase dephosphorylates, and negatively regulates the activities of, MAP kinases and MAP kinase kinases. It has been shown to inhibit the activation of p38 and JNK kinase cascades induced by environmental stresses. This phosphatase can also dephosphorylate cyclin-dependent kinases, and thus may be involved in cell cycle control. Overexpression of this phosphatase is reported to activate the expression of the tumor suppressor gene TP53/p53, which leads to G2/M cell cycle arrest and apoptosis. Three alternatively spliced transcript variants encoding distinct isoforms have been described.

UOM: 1 * 100 µl

Promoción

Proveedor: Biotium

Descripción: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Proveedor: Biotium

Descripción: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Numero del catalogo: (BNUM0710-50)

Proveedor: Biotium

Descripción: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

UOM: 1 * 50 µl

Promoción

Proveedor: Biotium

Descripción: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.

Proveedor: Biotium

Descripción: The c-Myc protein is a transcription factor, which is encoded by the c-Myc gene on human chromosome 8q24. c-Myc is commonly activated in a variety of tumor cells and plays an important role in cellular proliferation, differentiation, apoptosis and cell cycle progression. The phosphorylation of c-Myc has been investigated and previous studies have suggested a functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK) in cell proliferation and cell cycle regulation. Studies also have shown that c-Myc is essential for tumor cell development in vasculogenesis and angiogenesis that distribute blood throughout the cells, and which brought extensive attention in the development of new therapeutic approach for cancer treatment.