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anti-Human JAK1 Antibodies:
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Human Polyclonal JAK1 Primary Antibody for ELISA, ICC - ABIN6255762
Bai, Wang, Han, Xie, Ji, Yin, Chen, Wang, Jiang, Qi, Jiang: BCL2L10 inhibits growth and metastasis of hepatocellular carcinoma both in vitro and in vivo. in Molecular carcinogenesis 2017
Show all 3 Pubmed References
Human Polyclonal JAK1 Primary Antibody for IHC - ABIN966428
Wang, Griffin, Small, Thompson: Mechanism of Janus kinase 3-catalyzed phosphorylation of a Janus kinase 1 activation loop peptide. in Archives of biochemistry and biophysics 2003
Show all 2 Pubmed References
Human Polyclonal JAK1 Primary Antibody for IHC, WB - ABIN362146
Zheng, Hu, Quinn, Wang: Phosphotyrosine proteomic study of interferon alpha signaling pathway using a combination of immunoprecipitation and immobilized metal affinity chromatography. in Molecular & cellular proteomics : MCP 2005
Show all 4 Pubmed References
Human Polyclonal JAK1 Primary Antibody for ELISA, ICC - ABIN6262699
Chen, Zhou, Liu, Huang, Liu, Kang, Chen, Guo, Zhu, Sun: Combination of gemcitabine and erlotinib inhibits recurrent pancreatic cancer growth in mice via the JAK-STAT pathway. in Oncology reports 2018
Show all 2 Pubmed References
Human Polyclonal JAK1 Primary Antibody for IHC, WB - ABIN362702
Liu, Huang, Zeng, Chen, Huang, Guo, Liu, Xu, Mo, Li: Down-regulation of JAK1 by RNA interference inhibits growth of the lung cancer cell line A549 and interferes with the PI3K/mTOR pathway. in Journal of cancer research and clinical oncology 2011
Show all 3 Pubmed References
These findings clarify JAK1 signalling mechanisms and demonstrate a critical function of JAK1 in protection against mycobacterial infection and possibly the immunological surveillance of cancer.
Study concluded that JAK1 plays a role in the pathogenesis of both vitiligo (show MITF Antibodies) and psoriasis based on its upregulated level before treatment and downregulated level after treatment.
High JAK1 expression is associated with metastasis of pancreatic ductal adenocarcinoma.
IL6 (show IL6 Antibodies) family cytokine oncostatin-M (OSM (show OSM Antibodies)) induced a switch to the EMT (show ITK Antibodies) phenotype and protected cells from targeted drug-induced apoptosis in OSM (show OSM Antibodies) receptors (OSMRs)/JAK1/STAT3 (show STAT3 Antibodies)-dependent manner
Amorfrutin A also inhibited activation of the upstream kinases Janus-activated kinase 1 (JAK1), JAK2 (show JAK2 Antibodies) and Src (show SRC Antibodies) signaling pathways.
Jak1 is required for the survival of anaplastic large cell lymphoma.Jak1 mutations in anaplastic large cell lymphoma.
The good consonance between the docking results and CoMFA/CoMSIA contour maps provides helpful clues about the reasonable modification of molecules in order to design more efficient JAK 1 inhibitors. The developed models are expected to provide some directives for further synthesis of highly effective JAK 1 inhibitors.
Here we report a molecular mechanism by which JAK1 contributes to the malignant phenotype of activated B-cell diffuse large B-cell lymphoma (ABC (show ABCB6 Antibodies) DLBCL). Epigenetic regulation by JAK1 plays a prominent role in the gene expression program of ABC (show ABCB6 Antibodies) DLBCL cells by phosphorylating chromatin on H3Y41. The chromatin of nearly 3,000 genes had JAK1-dependent H3Y41 phosphorylation marks and required JAK1 for their expression.
miR (show MLXIP Antibodies)-30e has a critical role in the suppression of hepatocellular carcinoma (HCC (show FAM126A Antibodies)) and presents a novel mechanism of miRNA-mediated JAK1 expression in cancer cells that might be a good prognostic marker for survival of HCC (show FAM126A Antibodies) patients.
We demonstrate that impaired recruitment of CD11b (show ITGAM Antibodies)(+) myeloid cells with a JAK1/2 inhibitor inhibits glioma progression in vivo and prolongs survival in a murine glioma model.
Blockade of JAK1-JAK3 (show JAK3 Antibodies) accelerated, and selective inactivation of STAT3 (show STAT3 Antibodies) decelerated differentiation of progenitor cells.
Downregulated SOCS1 (show SOCS1 Antibodies) expression activates the JAK1/STAT1 (show STAT1 Antibodies) pathway and promotes polarization of macrophages into M1 type.
Jak1-deficient hematopoietic stem cells exhibit increased quiescence, an inability to enter the cell cycle in response to hematopoietic stress, and a marked reduction in cytokine sensing, including in response to type I interferons and IL-3 (show IL-3 Antibodies).
In this study, chronic UVB irradiation induced the expression of IL-10 (show IL10 Antibodies) and JAK1 that eventually activates the STAT3 (show STAT3 Antibodies) which leads to the transcription of proliferative and antiapoptotic markers.
findings reveal a mechanism by which JAK1 function and inflammatory signaling may be suppressed in response to metabolic stress and provide a mechanistic rationale for the investigation of AMPK (show PRKAA1 Antibodies) activators in a range of diseases associated with enhanced activation of the JAK (show JAK3 Antibodies)-STAT (show STAT1 Antibodies) pathway.
JAK1-mediated signaling cascades in skin regulate the expression of proteases associated with the maintenance of skin barrier function and demonstrate that perturbation of these pathways can lead to the development of spontaneous pruritic dermatitis.
Small-scale in vivo screening identified several genes, including Cd109 (show CD109 Antibodies), that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 (show STAT3 Antibodies) as a critical, pharmacologically targetable effector of CD109 (show CD109 Antibodies)-driven lung cancer metastasis
a causal relationship between MLH1 (show MLH1 Antibodies)-deficiency and incidence of oncogenic point mutations in tyrosine kinases driving cell transformation and acquired resistance to kinase-targeted cancer therapies, is reported.
High JAK1 expression is associated with Hepatic Fibrosis.
findings demonstrate that clinically relevant doses of the JAK1/2 inhibitor ruxolitinib suppresses the harmful consequences of macrophage overactivation characterizing Hemophagocytic lymphohistiocytosis in 2 murine models.
JAK1 activating mutants are insufficient to drive hepatocellular carcinoma development in vivo.
Data indicate that transmissible gastroenteritis virus (TGEV) infection activates the janus kinase signal transducer and activator of the transcription 1 (JAK (show JAK3 Antibodies)-STAT1 (show STAT1 Antibodies)) signaling pathway.
This is the first report of the genetic polymorphisms of the JAK1 and STAT3 (show STAT3 Antibodies) genes and their associations with the incidence of non-specific digestive disorder in rabbits.
Janus kinase 1 (JAK1), is a member of a new class of protein-tyrosine kinases (PTK) characterized by the presence of a second phosphotransferase-related domain immediately N-terminal to the PTK domain. The second phosphotransferase domain bears all the hallmarks of a protein kinase, although its structure differs significantly from that of the PTK and threonine/serine kinase family members. JAK1 is a large, widely expressed membrane-associated phosphoprotein. JAK1 is involved in the interferon-alpha/beta and -gamma signal transduction pathways. The reciprocal interdependence between JAK1 and TYK2 activities in the interferon-alpha pathway, and between JAK1 and JAK2 in the interferon-gamma pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes. These kinases couple cytokine ligand binding to tyrosine phosphorylation of various known signaling proteins and of a unique family of transcription factors termed the signal transducers and activators of transcription, or STATs.
tyrosine-protein kinase JAK1
, jak1 kinase
, Janus protein tyrosine kinase 1
, Janus kinase 1 (a protein tyrosine kinase)
, tyrosine kinase JAK1
, protein tyrosine kinase
, Janus kinase 1
, Tyrosine-protein kinase Jak1
, tyrosine-protein kinase JAK1-like