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6-Hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside potentiated the inhibitory effect of IFN-alpha (show IFNA ELISA Kits) on hepatocellular carcinoma cell proliferation through activation of the JAK (show JAK3 ELISA Kits)/STAT (show STAT1 ELISA Kits) signaling pathway by inhibiting SOCS3 (show SOCS3 ELISA Kits) expression.
JAK1 frameshifts are loss of function alterations that represent a potential pan-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 (show CD274 ELISA Kits) expression and response to interferon gamma (show IFNG ELISA Kits), leading to primary resistance to PD-1 (show RPL17 ELISA Kits) blockade therapy.
This study demonstrates that the nuclear import of JAK1 is essential for the optimal fitness of ABC (show ABCB6 ELISA Kits) 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 (show JAK3 ELISA Kits)/STAT (show STAT1 ELISA Kits) 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 (show MLH1 ELISA Kits)-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 (show STAT1 ELISA Kits) and STAT2 (show STAT2 ELISA Kits) activity, indicating differentially targeting JAK (show JAK3 ELISA Kits)/STAT (show STAT1 ELISA Kits) signaling pathways.
In this study, chronic UVB irradiation induced the expression of IL-10 (show IL10 ELISA Kits) and JAK1 that eventually activates the STAT3 (show STAT3 ELISA Kits) 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 ELISA Kits) activators in a range of diseases associated with enhanced activation of the JAK (show JAK3 ELISA Kits)-STAT (show STAT1 ELISA Kits) 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 ELISA Kits), that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 (show STAT3 ELISA Kits) as a critical, pharmacologically targetable effector of CD109 (show CD109 ELISA Kits)-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 (show CUZD1 ELISA Kits) interacts with a complex containing JAK1/JAK2 (show JAK2 ELISA Kits) and STAT5 (show STAT5A ELISA Kits), downstream transducers of prolactin (show PRL ELISA Kits) 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 (show JAK2 ELISA Kits), and JAK3 (show JAK3 ELISA Kits) 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.
Porcine reproductive and respiratory syndrome virus -activated TAK-1 (show NR2C2 ELISA Kits) was essential for the activation of JNK (show MAPK8 ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits) pathways and IL-8 (show IL8 ELISA Kits) expression.
Data indicate that transmissible gastroenteritis virus (TGEV) infection activates the janus kinase signal transducer and activator of the transcription 1 (JAK (show JAK3 ELISA Kits)-STAT1 (show STAT1 ELISA Kits)) signaling pathway.
Data show that proinflammatory cytokines induction was ERK1/2 (show MAPK1/3 ELISA Kits) and JNK1 (show MAPK8 ELISA Kits)/2 dependent.
These data suggest that the p38 (show MAPK14 ELISA Kits) and JNK (show MAPK8 ELISA Kits) 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 (show MAPK8 ELISA Kits) plays an active role in fragmentation of pig oocytes and that p38 MAPK (show MAPK14 ELISA Kits) is not involved in this process
Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2 (show MAPK1/3 ELISA Kits), in the neuroretina and retinal arteries.
PP2A and AIP1 (show PDCD6IP ELISA Kits) cooperatively induce activation of ASK1 (show MAP3K5 ELISA Kits)-JNK (show MAPK8 ELISA Kits) signaling and vascular endothelial cell apoptosis.
Phorbol 12-myristate 13-acetate activation of ERK (show MAPK1 ELISA Kits) and JNK (show MAPK8 ELISA Kits) 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 (show STAT3 ELISA Kits) 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
, janus kinase 1
, protein tyrosine kinase
, Janus kinase 1
, Tyrosine-protein kinase Jak1
, tyrosine-protein kinase JAK1-like