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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
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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
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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
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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
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Human Polyclonal JAK1 Primary Antibody for WB - ABIN5518768
Liu, Li, Liang, Li, Jiang, Chu, Yang: Hydrogen sulfide attenuates myocardial fibrosis in diabetic rats through the JAK/STAT signaling pathway. in International journal of molecular medicine 2018
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
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Human Polyclonal JAK1 Primary Antibody for WB - ABIN6242900
Feng, Chen, Wang, Cheng, Zou, Zhong, Xu: Roflumilast reverses polymicrobial sepsis-induced liver damage by inhibiting inflammation in mice. in Laboratory investigation; a journal of technical methods and pathology 2017
Human Polyclonal JAK1 Primary Antibody for WB - ABIN6242901
Yang, Shen, Xu, Yang, Tsai, Keng, Chen, Lee: Enhancing NK cell-mediated cytotoxicity to cisplatin-resistant lung cancer cells via MEK/Erk signaling inhibition. in Scientific reports 2017
Low-dose radiation decreases tumor progression via the inhibition of the JAK1/STAT3 signaling axis in breast cancer cell lines and in a mouse xenograft model.
Case Report: breast implant-associated anaplastic large cell lymphoma with dual JAK1/STAT3 mutations.
A small drug acting as a JAK1/2 inhibitor may also counteract the repressing effects of IL-6.
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.
In the Title.
Study concluded that JAK1 plays a role in the pathogenesis of both vitiligo 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 family cytokine oncostatin-M (OSM) induced a switch to the EMT phenotype and protected cells from targeted drug-induced apoptosis in OSM receptors (OSMRs)/JAK1/STAT3-dependent manner
Amorfrutin A also inhibited activation of the upstream kinases Janus-activated kinase 1 (JAK1), JAK2 and Src 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 DLBCL). Epigenetic regulation by JAK1 plays a prominent role in the gene expression program of ABC 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-30e has a critical role in the suppression of hepatocellular carcinoma (HCC) and presents a novel mechanism of miRNA-mediated JAK1 expression in cancer cells that might be a good prognostic marker for survival of HCC patients.
We demonstrate that impaired recruitment of CD11b(+) myeloid cells with a JAK1/2 inhibitor inhibits glioma progression in vivo and prolongs survival in a murine glioma model.
Whole-exome sequencing on patients with acute lymphoblastic leukemia (ALL) and discovered a somatic JAK1 S646P mutation. Functional studies demonstrated that only JAK1 S646P mutation could activate multiple signaling pathways, drive cytokine-independent cell growth, and promote proliferation of malignant cells in nude mice.
we have identified acquired activating mutations in JAK1 and STAT3 in two cases of effusion-limited BIA-ALCL and identified a possible contribution to disease development from a germline JAK3 variant.
JAK1 mutations are highly frequent in microsatellite unstable endometrial cancer, not associated with survival, but are associated with impaired upregulation of LMP7 and HLA class I and may therefore facilitate immune escape
We found that a significant higher gastric cancer risk was associated with IL-6 rs2069837G variant genotypes and JAK1 rs2230587A variant genotypes
6-Hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside potentiated the inhibitory effect of IFN-alpha on hepatocellular carcinoma cell proliferation through activation of the JAK/STAT signaling pathway by inhibiting SOCS3 expression.
JAK1 frameshifts are loss of function alterations that represent a potential pan-cancer adaptation to immune responses against tumors with microsatellite instability
these data suggest that aloin attenuated LPSinduced inflammation by inhibiting ROSmediated activation of the JAK1STAT1/3 signalling pathway, thereby inhibiting the nuclear translocation of STAT1/3 in RAW264.7 cells.
Blockade of JAK1-JAK3 accelerated, and selective inactivation of STAT3 decelerated differentiation of progenitor cells.
Downregulated SOCS1 expression activates the JAK1/STAT1 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.
In this study, chronic UVB irradiation induced the expression of IL-10 and JAK1 that eventually activates the STAT3 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 activators in a range of diseases associated with enhanced activation of the JAK-STAT 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, that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 as a critical, pharmacologically targetable effector of CD109-driven lung cancer metastasis
a causal relationship between MLH1-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.
Data show that CUZD1 interacts with a complex containing JAK1/JAK2 and STAT5, downstream transducers of prolactin signaling in the mammary gland.
JAK1 conditional knockout mice will be an invaluable tool to study cytokine signaling during normal development and disease progression in adult animals.
JAK1, JAK2, and JAK3 are involved in stimulation of functional activity of mesenchymal progenitor cells by fibroblast growth factor.
JAK mediated signaling is involved in the differentiation and proliferation of mesenchymal progenitor cells.
Data indicate thar Janus kinase 1 (Jak1) degradation is dependent on Nedd4 family interacting proteins Ndfip1/Ndfip2.
Experiments implicate JAK1/3 signaling in cancer- and myocardial infarction-mediated diaphragm weakness in mice.
JAK1/JAK2 inhibition of graft-versus-host disease was associated with the modulation of chemokine receptor expression, which may have been one factor in the reduced infiltration of donor T cells in graft-versus-host disease target organs.
-1 promotes IFN-alpha-induced autophagy via the JAK1-STAT1 signaling.
Zn deficiency enhances the acute phase response and particularly the JAK-STAT3 pathway, resulting in increased serum amyloid A production.
JAK1 activating mutants are insufficient to drive hepatocellular carcinoma development in vivo.
Required for cell migration of anterior mesendoderm during gastrulation, resulting in extension of the anterior body axis. MO/dominant negative expression gives identical morphotype/phenotype to STAT3alpha knockdown.
Data indicate that transmissible gastroenteritis virus (TGEV) infection activates the janus kinase signal transducer and activator of the transcription 1 (JAK-STAT1) signaling pathway.
This is the first report of the genetic polymorphisms of the JAK1 and STAT3 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