Ignet

Gene Information

Gene symbol: JAK2

Gene name: Janus kinase 2

HGNC ID: 6192

Synonyms: JTK10

Related Genes

#	Gene Symbol	Number of hits
1	CD274	1 hits
2	CD34	1 hits
3	HLA-A	1 hits
4	IFNB1	1 hits
5	IFNG	1 hits
6	IL12A	1 hits
7	JAK1	1 hits
8	JAK3	1 hits
9	STAT1	1 hits
10	STAT2	1 hits
11	STAT3	1 hits
12	TYK2	1 hits
13	WT1	1 hits

Related Sentences

#	PMID	Sentence
1	16533527	Fifty HLA-A*0201 peptides were selected from several target oncoproteins: Wilms' tumor protein (WT1), native and imatinib-mutated bcr-abl p210, JAK2 protein and Ewing's sarcoma fusion protein type 1.
2	19656875	Analyses of cells infected with VEEV and VEEV replicon particles (VRP) demonstrate that viral infection rapidly disrupts tyrosine phosphorylation and nuclear translocation of the transcription factor STAT1 in response to both IFN-beta and IFN-gamma.
3	19656875	Furthermore, at times when STAT1 activation was efficiently inhibited, VRP infection did not limit tyrosine phosphorylation of Jak1, Tyk2, or STAT2 after IFN-beta treatment but did inhibit Jak1 and Jak2 activation in response to IFN-gamma, suggesting that VEEV interferes with STAT1 activation by the type I and II receptor complexes through distinct mechanisms.
4	20372811	Interleukin-12-anchored exosomes increase cytotoxicity of T lymphocytes by reversing the JAK/STAT pathway impaired by tumor-derived exosomes.
5	20372811	We investigated whether interleukin-12 (IL-12)-anchored exosomes (EXO/IL-12) reverse tumor exosome-mediated inhibition of T-cell activation and cytotoxicity was associated with inhibition of JAK3 and p-STAT5.
6	20372811	A co-expression plasmid of pBudCE4.1/IL-12A/ IL-12B-GPI was constructed.
7	20372811	Expression of JAK2, JAK3 and p-STAT5 was detected by Western blotting.
8	20372811	Our results showed that EXO/IL-12 was much more efficient in induction of the proliferation, release of IFN-gamma and cytotoxic effect of T lymphocytes than conventional exosomes in vitro.
9	20372811	Exosomes inhibited the expression of JAK3 and phosphorylation of STAT5 in high doses in T-cells, but not JAK2, while EXO/IL-12 had much less attenuated reduction of the expression of p-STAT5.
10	20372811	The enhanced cytotoxic effects of T lymphocytes might partly depend on EXO/IL-12 reversing the suppressed expression of p-Stat5 by Jak2/Stat5 pathway.
11	20372811	Interleukin-12-anchored exosomes increase cytotoxicity of T lymphocytes by reversing the JAK/STAT pathway impaired by tumor-derived exosomes.
12	20372811	We investigated whether interleukin-12 (IL-12)-anchored exosomes (EXO/IL-12) reverse tumor exosome-mediated inhibition of T-cell activation and cytotoxicity was associated with inhibition of JAK3 and p-STAT5.
13	20372811	A co-expression plasmid of pBudCE4.1/IL-12A/ IL-12B-GPI was constructed.
14	20372811	Expression of JAK2, JAK3 and p-STAT5 was detected by Western blotting.
15	20372811	Our results showed that EXO/IL-12 was much more efficient in induction of the proliferation, release of IFN-gamma and cytotoxic effect of T lymphocytes than conventional exosomes in vitro.
16	20372811	Exosomes inhibited the expression of JAK3 and phosphorylation of STAT5 in high doses in T-cells, but not JAK2, while EXO/IL-12 had much less attenuated reduction of the expression of p-STAT5.
17	20372811	The enhanced cytotoxic effects of T lymphocytes might partly depend on EXO/IL-12 reversing the suppressed expression of p-Stat5 by Jak2/Stat5 pathway.
18	20372811	Interleukin-12-anchored exosomes increase cytotoxicity of T lymphocytes by reversing the JAK/STAT pathway impaired by tumor-derived exosomes.
19	20372811	We investigated whether interleukin-12 (IL-12)-anchored exosomes (EXO/IL-12) reverse tumor exosome-mediated inhibition of T-cell activation and cytotoxicity was associated with inhibition of JAK3 and p-STAT5.
20	20372811	A co-expression plasmid of pBudCE4.1/IL-12A/ IL-12B-GPI was constructed.
21	20372811	Expression of JAK2, JAK3 and p-STAT5 was detected by Western blotting.
22	20372811	Our results showed that EXO/IL-12 was much more efficient in induction of the proliferation, release of IFN-gamma and cytotoxic effect of T lymphocytes than conventional exosomes in vitro.
23	20372811	Exosomes inhibited the expression of JAK3 and phosphorylation of STAT5 in high doses in T-cells, but not JAK2, while EXO/IL-12 had much less attenuated reduction of the expression of p-STAT5.
24	20372811	The enhanced cytotoxic effects of T lymphocytes might partly depend on EXO/IL-12 reversing the suppressed expression of p-Stat5 by Jak2/Stat5 pathway.
25	20739538	The adult mouse neurovirulent strain AR86 was found to rapidly and robustly inhibit tyrosine phosphorylation of STAT1 and STAT2 in response to IFN-γ and/or IFN-β.
26	20739538	Decreased STAT activation in AR86-infected cells was associated with decreased activation of the IFN receptor-associated tyrosine kinases Tyk2, Jak1, and Jak2.
27	24324467	IL-6, Prostaglandin-E2, and IL-10 were identified as factors in cultures of primary human tumors responsible for the inhibited development and activation of skin DC as well as monocyte-derived DC.
28	24324467	Mostly from mouse studies, the JAK2/STAT3 signaling pathway has emerged as a "master switch" of tumor-induced immune suppression.
29	26155422	Interferon-γ-induced activation of JAK1 and JAK2 suppresses tumor cell susceptibility to NK cells through upregulation of PD-L1 expression.
30	26155422	Inhibition of JAK1 or JAK2 in human tumor cells was previously shown to increase susceptibility of these cells to NK cell lysis.
31	26155422	Incubation of tumor cells with supernatant from activated NK cells or interferon-gamma (IFNγ)-induced activation of pSTAT1 and increased expression of PD-L1 without altering expression of other activating or inhibitory NK cell ligands.
32	26155422	These functional effects were blocked by chemical JAK inhibition or shRNAs targeting JAK1, JAK2 or STAT1.
33	26155422	These results show that NK cell activation and secretion of IFNγ results in activation of JAK1, JAK2 and STAT1 in tumor cells, resulting in rapid up-regulation of PD-L1 expression.
34	26155422	These observations suggest that JAK pathway inhibitors as well as PD-1 and PD-L1 antibodies may work synergistically with other immune therapies by preventing IFN-induced inhibition of NK cell-mediated tumor cell lysis.
35	26155422	Interferon-γ-induced activation of JAK1 and JAK2 suppresses tumor cell susceptibility to NK cells through upregulation of PD-L1 expression.
36	26155422	Inhibition of JAK1 or JAK2 in human tumor cells was previously shown to increase susceptibility of these cells to NK cell lysis.
37	26155422	Incubation of tumor cells with supernatant from activated NK cells or interferon-gamma (IFNγ)-induced activation of pSTAT1 and increased expression of PD-L1 without altering expression of other activating or inhibitory NK cell ligands.
38	26155422	These functional effects were blocked by chemical JAK inhibition or shRNAs targeting JAK1, JAK2 or STAT1.
39	26155422	These results show that NK cell activation and secretion of IFNγ results in activation of JAK1, JAK2 and STAT1 in tumor cells, resulting in rapid up-regulation of PD-L1 expression.
40	26155422	These observations suggest that JAK pathway inhibitors as well as PD-1 and PD-L1 antibodies may work synergistically with other immune therapies by preventing IFN-induced inhibition of NK cell-mediated tumor cell lysis.
41	26155422	Interferon-γ-induced activation of JAK1 and JAK2 suppresses tumor cell susceptibility to NK cells through upregulation of PD-L1 expression.
42	26155422	Inhibition of JAK1 or JAK2 in human tumor cells was previously shown to increase susceptibility of these cells to NK cell lysis.
43	26155422	Incubation of tumor cells with supernatant from activated NK cells or interferon-gamma (IFNγ)-induced activation of pSTAT1 and increased expression of PD-L1 without altering expression of other activating or inhibitory NK cell ligands.
44	26155422	These functional effects were blocked by chemical JAK inhibition or shRNAs targeting JAK1, JAK2 or STAT1.
45	26155422	These results show that NK cell activation and secretion of IFNγ results in activation of JAK1, JAK2 and STAT1 in tumor cells, resulting in rapid up-regulation of PD-L1 expression.
46	26155422	These observations suggest that JAK pathway inhibitors as well as PD-1 and PD-L1 antibodies may work synergistically with other immune therapies by preventing IFN-induced inhibition of NK cell-mediated tumor cell lysis.
47	26155422	Interferon-γ-induced activation of JAK1 and JAK2 suppresses tumor cell susceptibility to NK cells through upregulation of PD-L1 expression.
48	26155422	Inhibition of JAK1 or JAK2 in human tumor cells was previously shown to increase susceptibility of these cells to NK cell lysis.
49	26155422	Incubation of tumor cells with supernatant from activated NK cells or interferon-gamma (IFNγ)-induced activation of pSTAT1 and increased expression of PD-L1 without altering expression of other activating or inhibitory NK cell ligands.
50	26155422	These functional effects were blocked by chemical JAK inhibition or shRNAs targeting JAK1, JAK2 or STAT1.
51	26155422	These results show that NK cell activation and secretion of IFNγ results in activation of JAK1, JAK2 and STAT1 in tumor cells, resulting in rapid up-regulation of PD-L1 expression.
52	26155422	These observations suggest that JAK pathway inhibitors as well as PD-1 and PD-L1 antibodies may work synergistically with other immune therapies by preventing IFN-induced inhibition of NK cell-mediated tumor cell lysis.
53	26275051	The microarray analyses of the CD34+ cells and granulocytes were performed from 20 de novo MPN subjects: JAK2 positive ET, PV, PMF subjects, and JAK2 negative ET/PMF subjects.
54	26275051	Thirty-six genes (including RUNX1, TNFRSF19) were persistently highly expressed, while 42 genes (including FOXD4, PDE4A) were underexpressed both in CD34+ cells and granulocytes.
55	26275051	Using proteomic studies, significant up-regulation was observed for MAPK and PI3K/AKT signaling regulators that control myeloid cell apoptosis and proliferation: RAC2, MNDA, S100A8/9, CORO1A, and GNAI2.
56	26275051	When the status of the mTOR signaling pathway related genes was analyzed, PI3K/AKT regulators were preferentially up-regulated in CD34+ cells of MPNs, with down-regulated major components of the protein complex EIF4F.
57	26275051	Molecular profiling of CD34+ cells and granulocytes of MPN determined gene expression patterns beyond their recognized function in disease pathogenesis that included dominant up-regulation of PI3K/AKT signaling.