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JAK1 mutations are highly frequent in microsatellite unstable endometrial cancer, not associated with survival, but are associated with impaired upregulation of LMP7 (Montrer PSMB8 Kits ELISA) and HLA class I (Montrer MICA Kits ELISA) and may therefore facilitate immune escape
We found that a significant higher gastric cancer risk was associated with IL-6 (Montrer IL6 Kits ELISA) rs2069837G variant genotypes and JAK1 rs2230587A variant genotypes
6-Hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside potentiated the inhibitory effect of IFN-alpha (Montrer IFNA Kits ELISA) on hepatocellular carcinoma cell proliferation through activation of the JAK (Montrer JAK3 Kits ELISA)/STAT (Montrer STAT1 Kits ELISA) signaling pathway by inhibiting SOCS3 (Montrer SOCS3 Kits ELISA) 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 (Montrer CD274 Kits ELISA) expression and response to interferon gamma (Montrer IFNG Kits ELISA), leading to primary resistance to PD-1 (Montrer RPL17 Kits ELISA) blockade therapy.
This study demonstrates that the nuclear import of JAK1 is essential for the optimal fitness of ABC (Montrer ABCB6 Kits ELISA) 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 (Montrer JAK3 Kits ELISA)/STAT (Montrer STAT1 Kits ELISA) 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
In this study, chronic UVB irradiation induced the expression of IL-10 (Montrer IL10 Kits ELISA) and JAK1 that eventually activates the STAT3 (Montrer STAT3 Kits ELISA) 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 (Montrer PRKAA1 Kits ELISA) activators in a range of diseases associated with enhanced activation of the JAK (Montrer JAK3 Kits ELISA)-STAT (Montrer STAT1 Kits ELISA) 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 (Montrer CD109 Kits ELISA), that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 (Montrer STAT3 Kits ELISA) as a critical, pharmacologically targetable effector of CD109 (Montrer CD109 Kits ELISA)-driven lung cancer metastasis
a causal relationship between MLH1 (Montrer MLH1 Kits ELISA)-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 (Montrer CUZD1 Kits ELISA) interacts with a complex containing JAK1/JAK2 (Montrer JAK2 Kits ELISA) and STAT5 (Montrer STAT5A Kits ELISA), downstream transducers of prolactin (Montrer PRL Kits ELISA) 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 (Montrer JAK2 Kits ELISA), and JAK3 (Montrer JAK3 Kits ELISA) 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 (Montrer NR2C2 Kits ELISA) was essential for the activation of JNK (Montrer MAPK8 Kits ELISA) and NF-kappaB (Montrer NFKB1 Kits ELISA) pathways and IL-8 (Montrer IL8 Kits ELISA) expression.
Data indicate that transmissible gastroenteritis virus (TGEV) infection activates the janus kinase signal transducer and activator of the transcription 1 (JAK (Montrer JAK3 Kits ELISA)-STAT1 (Montrer STAT1 Kits ELISA)) signaling pathway.
Data show that proinflammatory cytokines induction was ERK1/2 (Montrer MAPK1/3 Kits ELISA) and JNK1 (Montrer MAPK8 Kits ELISA)/2 dependent.
These data suggest that the p38 (Montrer MAPK14 Kits ELISA) and JNK (Montrer MAPK8 Kits ELISA) 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 (Montrer MAPK8 Kits ELISA) plays an active role in fragmentation of pig oocytes and that p38 MAPK (Montrer MAPK14 Kits ELISA) is not involved in this process
Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2 (Montrer MAPK1/3 Kits ELISA), in the neuroretina and retinal arteries.
PP2A and AIP1 (Montrer PDCD6IP Kits ELISA) cooperatively induce activation of ASK1 (Montrer MAP3K5 Kits ELISA)-JNK (Montrer MAPK8 Kits ELISA) signaling and vascular endothelial cell apoptosis.
Phorbol 12-myristate 13-acetate activation of ERK (Montrer MAPK1 Kits ELISA) and JNK (Montrer MAPK8 Kits ELISA) 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 (Montrer STAT3 Kits ELISA) 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