JNK2 Protein, Human, Recombinant (His)

产品编号 TMPY-04550

别名: JNK2α, SAPK1a, PRKM9, JNK2β, JNK2, SAPK, JNK2BETA, mitogen-activated protein kinase 9, JNK2ALPHA, JNK-55, p54aSAPK, JNK2B, JNK2A, p54a

Mitogen-activated protein kinase 9 (MAPK9), also well known as c-Jun N-terminal kinase (JNK2), is a member of the MAP kinase subfamily belonging to the protein kinase superfamily. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating some transcription factors, such as c-Jun and ATF2. The crystal structure of human JNK2 complexed with an indazole inhibitor by applying a high-throughput protein engineering and surface-site mutagenesis approach. A novel conformation of the activation loop is observed, which is not compatible with its phosphorylation by upstream kinases. This activation inhibitory conformation of JNK2 is stabilized by the MAP kinase insert that interacts with the activation loop in an induced-fit manner. It suggests that the MAP kinase insert of JNK2 plays a role in the regulation of JNK2 activation, possibly by interacting with intracellular binding partners. JNK2 deficiency leads to reduced c-Jun degradation, thereby augmenting c-Jun levels and cellular proliferation, and suggests that JNK2 is a negative regulator of cellular proliferation in multiple cell types. JNK2 prevents replicative stress by coordinating cell cycle progression and DNA damage repair mechanisms. JNK2 blocks the ubiquitination of tumor suppressor p53, and thus increases the stability of p53 in nonstressed cells. JNK2 negatively regulates antigen-specific CD8+ T cell expansion and effector function, and thus selectively blocking JNK2 in CD8+ T cells may potentially enhance the anti-tumor immune response. Lack of JNK2 expression was associated with higher tumor aneuploidy and reduced DNA damage response. Additionally, the JNK2 protein could be a novel therapeutic target in dry eye disease and may provide a novel target for the prevention of vascular disease and atherosclerosis.

TargetMol的所有产品和服务仅用于科学研究，不能被用于人体，我们也不向个人提供产品和服务。

JNK2 Protein, Human, Recombinant (His)

规格	价格/CNY		货期	数量
50 μg	￥ 3,170		5日内发货
500 μg	￥ 20,800		5日内发货

大包装超大折扣，点击咨询

DATASHEET SDS

更多批次查询请联系客服

生物活性

技术参数

产品性质

参考文献

生物活性

No Kinase Activity

产品描述

种属	Human
表达系统	Baculovirus-Insect Cells
标签	His
蛋白编号	P45984-1
别名	JNK2α, SAPK1a, PRKM9, JNK2β, JNK2, SAPK, JNK2BETA, mitogen-activated protein kinase 9, JNK2ALPHA, JNK-55, p54aSAPK, JNK2B, JNK2A, p54a
蛋白构建	A DNA sequence encoding the full length of human MAPK9 (NP_002743.3) (Met 1-Arg 424) was fused with a polyhistidine tag at the C-terminus.
蛋白纯度	> 90 % as determined by SDS-PAGE
分子量	49.5 kDa (predicted)

内毒素	< 1.0 EU per μg of the protein as determined by the LAL method
缓冲液	Lyophilized from sterile 50mM Tris, 100mM NaCl, pH 8.0, 10% glycerol, 0. 5mM EDTA, 0. 5mM PMSFPlease contact us for any concerns or special requirements. Normally 5 % - 8 % trehalose, mannitol and 0. 01% Tween 80 are added as protectants before lyophilization. Please refer to the specific buffer information in the hard copy of CoA.
复溶方法	A hardcopy of datasheet with reconstitution instructions is sent along with the products. Please refer to it for detailed information.
存储	Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
运输方式	In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
研究背景	Mitogen-activated protein kinase 9 (MAPK9), also well known as c-Jun N-terminal kinase (JNK2), is a member of the MAP kinase subfamily belonging to the protein kinase superfamily. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating some transcription factors, such as c-Jun and ATF2. The crystal structure of human JNK2 complexed with an indazole inhibitor by applying a high-throughput protein engineering and surface-site mutagenesis approach. A novel conformation of the activation loop is observed, which is not compatible with its phosphorylation by upstream kinases. This activation inhibitory conformation of JNK2 is stabilized by the MAP kinase insert that interacts with the activation loop in an induced-fit manner. It suggests that the MAP kinase insert of JNK2 plays a role in the regulation of JNK2 activation, possibly by interacting with intracellular binding partners. JNK2 deficiency leads to reduced c-Jun degradation, thereby augmenting c-Jun levels and cellular proliferation, and suggests that JNK2 is a negative regulator of cellular proliferation in multiple cell types. JNK2 prevents replicative stress by coordinating cell cycle progression and DNA damage repair mechanisms. JNK2 blocks the ubiquitination of tumor suppressor p53, and thus increases the stability of p53 in nonstressed cells. JNK2 negatively regulates antigen-specific CD8+ T cell expansion and effector function, and thus selectively blocking JNK2 in CD8+ T cells may potentially enhance the anti-tumor immune response. Lack of JNK2 expression was associated with higher tumor aneuploidy and reduced DNA damage response. Additionally, the JNK2 protein could be a novel therapeutic target in dry eye disease and may provide a novel target for the prevention of vascular disease and atherosclerosis.