Use your antibodies-online credentials, if available.
抗Human JAK1 抗体:
抗Mouse (Murine) JAK1 抗体:
抗Rat (Rattus) JAK1 抗体:
Chicken Monoclonal JAK1 Primary Antibody for IF, IP - ABIN967842
Blesofsky, Mowen, Arduini, Baker, Murphy, Bowtell, David: Regulation of STAT protein synthesis by c-Cbl. in Oncogene 2001
Show all 5 Pubmed References
Chicken Monoclonal JAK1 Primary Antibody for IF, IP - ABIN967841
Kawazoe, Naka, Fujimoto, Kohzaki, Morita, Narazaki, Okumura, Saitoh, Nakagawa, Uchiyama, Akira, Kishimoto: Signal transducer and activator of transcription (STAT)-induced STAT inhibitor 1 (SSI-1)/suppressor of cytokine signaling 1 (SOCS1) inhibits insulin signal transduction pathway through modulating insulin receptor substrate 1 (IRS-1) phosphorylation. in The Journal of experimental medicine 2001
Show all 5 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 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
miR (显示 MLXIP 抗体)-30e has a critical role in the suppression of hepatocellular carcinoma (HCC (显示 FAM126A 抗体)) and presents a novel mechanism of miRNA-mediated JAK1 expression in cancer cells that might be a good prognostic marker for survival of HCC (显示 FAM126A 抗体) patients.
We demonstrate that impaired recruitment of CD11b (显示 ITGAM 抗体)(+) 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 (显示 STAT3 抗体) in two cases of effusion-limited BIA-ALCL and identified a possible contribution to disease development from a germline JAK3 (显示 JAK3 抗体) variant.
JAK1 mutations are highly frequent in microsatellite unstable endometrial cancer, not associated with survival, but are associated with impaired upregulation of LMP7 (显示 PSMB8 抗体) and HLA class I (显示 MICA 抗体) and may therefore facilitate immune escape
We found that a significant higher gastric cancer risk was associated with IL-6 (显示 IL6 抗体) rs2069837G variant genotypes and JAK1 rs2230587A variant genotypes
6-Hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside potentiated the inhibitory effect of IFN-alpha (显示 IFNA 抗体) on hepatocellular carcinoma cell proliferation through activation of the JAK (显示 JAK3 抗体)/STAT (显示 STAT1 抗体) signaling pathway by inhibiting SOCS3 (显示 SOCS3 抗体) expression.
JAK1 frameshifts are loss of function alterations that represent a potential pan (显示 SUPT6H 抗体)-cancer adaptation to immune responses against tumors with microsatellite instability
Study provides evidence that JAK1/2 loss-of-function mutations are a genetic mechanism of lack of reactive PD-L1 (显示 CD274 抗体) expression and response to interferon gamma (显示 IFNG 抗体), leading to primary resistance to PD-1 (显示 PDCD1 抗体) blockade therapy.
This study demonstrates that the nuclear import of JAK1 is essential for the optimal fitness of ABC (显示 ABCB6 抗体) DLBCL cells.
In this study, chronic UVB irradiation induced the expression of IL-10 (显示 IL10 抗体) and JAK1 that eventually activates the STAT3 (显示 STAT3 抗体) 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 (显示 PRKAA1 抗体) activators in a range of diseases associated with enhanced activation of the JAK (显示 JAK3 抗体)-STAT (显示 STAT1 抗体) 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 (显示 CD109 抗体), that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 (显示 STAT3 抗体) as a critical, pharmacologically targetable effector of CD109 (显示 CD109 抗体)-driven lung cancer metastasis
a causal relationship between MLH1 (显示 MLH1 抗体)-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 (显示 CUZD1 抗体) interacts with a complex containing JAK1/JAK2 (显示 JAK2 抗体) and STAT5 (显示 STAT5A 抗体), downstream transducers of prolactin (显示 PRL 抗体) 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 (显示 JAK2 抗体), and JAK3 (显示 JAK3 抗体) are involved in stimulation of functional activity of mesenchymal progenitor cells by fibroblast growth factor.
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 (显示 JAK3 抗体)-STAT1 (显示 STAT1 抗体)) signaling pathway.
This is the first report of the genetic polymorphisms of the JAK1 and STAT3 (显示 STAT3 抗体) 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