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miR (show MLXIP Proteins)-30e has a critical role in the suppression of hepatocellular carcinoma (HCC (show FAM126A Proteins)) and presents a novel mechanism of miRNA-mediated JAK1 expression in cancer cells that might be a good prognostic marker for survival of HCC (show FAM126A Proteins) patients.
We demonstrate that impaired recruitment of CD11b (show ITGAM Proteins)(+) 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 (show STAT3 Proteins) in two cases of effusion-limited BIA-ALCL and identified a possible contribution to disease development from a germline JAK3 (show JAK3 Proteins) variant.
JAK1 mutations are highly frequent in microsatellite unstable endometrial cancer, not associated with survival, but are associated with impaired upregulation of LMP7 (show PSMB8 Proteins) and HLA class I (show MICA Proteins) and may therefore facilitate immune escape
We found that a significant higher gastric cancer risk was associated with IL-6 (show IL6 Proteins) rs2069837G variant genotypes and JAK1 rs2230587A variant genotypes
6-Hydroxy-3-O-methyl-kaempferol 6-O-glucopyranoside potentiated the inhibitory effect of IFN-alpha (show IFNA Proteins) on hepatocellular carcinoma cell proliferation through activation of the JAK (show JAK3 Proteins)/STAT (show STAT1 Proteins) signaling pathway by inhibiting SOCS3 (show SOCS3 Proteins) 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 Proteins) expression and response to interferon gamma (show IFNG Proteins), leading to primary resistance to PD-1 (show PDCD1 Proteins) blockade therapy.
This study demonstrates that the nuclear import of JAK1 is essential for the optimal fitness of ABC (show ABCB6 Proteins) DLBCL cells.
In this study, chronic UVB irradiation induced the expression of IL-10 (show IL10 Proteins) and JAK1 that eventually activates the STAT3 (show STAT3 Proteins) 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 Proteins) activators in a range of diseases associated with enhanced activation of the JAK (show JAK3 Proteins)-STAT (show STAT1 Proteins) 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 Proteins), that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 (show STAT3 Proteins) as a critical, pharmacologically targetable effector of CD109 (show CD109 Proteins)-driven lung cancer metastasis
a causal relationship between MLH1 (show MLH1 Proteins)-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 (show CUZD1 Proteins) interacts with a complex containing JAK1/JAK2 (show JAK2 Proteins) and STAT5 (show STAT5A Proteins), downstream transducers of prolactin (show PRL Proteins) 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 Proteins), and JAK3 (show JAK3 Proteins) 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 (show JAK3 Proteins)-STAT1 (show STAT1 Proteins)) signaling pathway.
This is the first report of the genetic polymorphisms of the JAK1 and STAT3 (show STAT3 Proteins) 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