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Porcine reproductive and respiratory syndrome virus -activated TAK-1 (显示 NR2C2 ELISA试剂盒) was essential for the activation of JNK (显示 MAPK8 ELISA试剂盒) and NF-kappaB (显示 NFKB1 ELISA试剂盒) pathways and IL-8 (显示 IL8 ELISA试剂盒) expression.
Data indicate that transmissible gastroenteritis virus (TGEV) infection activates the janus kinase signal transducer and activator of the transcription 1 (JAK (显示 JAK3 ELISA试剂盒)-STAT1 (显示 STAT1 ELISA试剂盒)) signaling pathway.
Data show that proinflammatory cytokines induction was ERK1/2 (显示 MAPK1/3 ELISA试剂盒) and JNK1 (显示 MAPK8 ELISA试剂盒)/2 dependent.
These data suggest that the p38 (显示 MAPK14 ELISA试剂盒) and JNK (显示 MAPK8 ELISA试剂盒) signaling pathways play pivotal roles in PRRSV replication and may regulate immune responses during virus infection.
based on the data, we can conclude that JNK (显示 MAPK8 ELISA试剂盒) plays an active role in fragmentation of pig oocytes and that p38 MAPK (显示 MAPK14 ELISA试剂盒) is not involved in this process
Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2 (显示 MAPK1/3 ELISA试剂盒), in the neuroretina and retinal arteries.
PP2A and AIP1 (显示 PDCD6IP ELISA试剂盒) cooperatively induce activation of ASK1 (显示 MAP3K5 ELISA试剂盒)-JNK (显示 MAPK8 ELISA试剂盒) signaling and vascular endothelial cell apoptosis.
Phorbol 12-myristate 13-acetate activation of ERK (显示 MAPK1 ELISA试剂盒) and JNK (显示 MAPK8 ELISA试剂盒) signaling is relevant in the regulation of gene expression during follicular development, ovulation, and luteinization.
This is the first report of the genetic polymorphisms of the JAK1 and STAT3 (显示 STAT3 ELISA试剂盒) genes and their associations with the incidence of non-specific digestive disorder in rabbits.
IL-11 (显示 IL11 ELISA试剂盒) induces the expression of MMP-13 (显示 MMP13 ELISA试剂盒) in gastric cancer SCH (显示 NF2 ELISA试剂盒) cells partly via the PI3K (显示 PIK3CA ELISA试剂盒)-AKT (显示 AKT1 ELISA试剂盒) and JAK (显示 JAK3 ELISA试剂盒)-STAT3 (显示 STAT3 ELISA试剂盒) pathways.
Study provides evidence that JAK1/2 loss-of-function mutations are a genetic mechanism of lack of reactive PD-L1 (显示 CD274 ELISA试剂盒) expression and response to interferon gamma (显示 IFNG ELISA试剂盒), leading to primary resistance to PD-1 (显示 RPL17 ELISA试剂盒) blockade therapy.
This study demonstrates that the nuclear import of JAK1 is essential for the optimal fitness of ABC (显示 ABCB6 ELISA试剂盒) DLBCL cells.
JAK1 rs11576173 and rs1497056 genotypes were significantly related to severe necroinflammatory activity (NIA) grade of chronic hepatitis C patients.
Multiple myeloma cells over express JAK1/2 and suggest combined chemotherapy with ruxolitinib, bortezomib and lenalidomide to inhibit JAK (显示 JAK3 ELISA试剂盒)/STAT (显示 STAT1 ELISA试剂盒) pathway.
Mechanistic investigations reveal that AJUBA specifically binds the FERM domain of JAK1 to dissociate JAK1 from the IFNgamma recepter, resulting in an inhibition of STAT1 phosporylation and concomitantly its nuclear translocation. Clinically, the level of AJUBA in CRC specimens is negatively correlated with the levels of IFIT2 and pSTAT1
Multilevel genomic analyses of microsatellite instability+ colorectal cancer revealed molecular heterogeneity with clinical relevance, including tumor immunogenicity and a favorable patient outcome associated with JAK1 mutations and the transcriptomic subgroup CMS1
a causal relationship between MLH1 (显示 MLH1 ELISA试剂盒)-deficiency and incidence of oncogenic point mutations in tyrosine kinases driving cell transformation and acquired resistance to kinase-targeted cancer therapies, is reported.
Data show that moringin (GMG-ITC) had a limited inhibitory effect on IFNalpha-induced STAT1 (显示 STAT1 ELISA试剂盒) and STAT2 (显示 STAT2 ELISA试剂盒) activity, indicating differentially targeting JAK (显示 JAK3 ELISA试剂盒)/STAT (显示 STAT1 ELISA试剂盒) signaling pathways.
our studies highlight Jak1 as the first identified substrate for USP6 (显示 USP6 ELISA试剂盒), and they offer a mechanistic rationale for the clinical investigation of Jak (显示 JAK3 ELISA试剂盒) and STAT3 (显示 STAT3 ELISA试剂盒) inhibitors as therapeutics for the treatment of bone and soft tissue tumors along with other neoplasms driven by USP6 (显示 USP6 ELISA试剂盒) overexpression
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 ELISA试剂盒) activators in a range of diseases associated with enhanced activation of the JAK (显示 JAK3 ELISA试剂盒)-STAT (显示 STAT1 ELISA试剂盒) pathway.
CD109 (显示 CD109 ELISA试剂盒) drives lung adenocarcinoma metastasis in a JAK (显示 JAK3 ELISA试剂盒)-STAT (显示 STAT1 ELISA试剂盒)-dependent manner.Inhibition of JAK (显示 JAK3 ELISA试剂盒) or CD109 (显示 CD109 ELISA试剂盒) may be a potential therapeutic strategy to prevent metastasis
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 ELISA试剂盒), that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 (显示 STAT3 ELISA试剂盒) as a critical, pharmacologically targetable effector of CD109 (显示 CD109 ELISA试剂盒)-driven lung cancer metastasis
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 ELISA试剂盒) interacts with a complex containing JAK1/JAK2 (显示 JAK2 ELISA试剂盒) and STAT5 (显示 STAT5A ELISA试剂盒), downstream transducers of prolactin (显示 PRL ELISA试剂盒) 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 ELISA试剂盒), and JAK3 (显示 JAK3 ELISA试剂盒) 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.
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
, janus kinase 1
, protein tyrosine kinase
, Janus kinase 1
, Tyrosine-protein kinase Jak1
, tyrosine-protein kinase JAK1-like