STAT4


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STAT4

A gene on chromosome 17q21.31 that encodes a member of the STAT family of transcription factors, which are phosphorylated by receptor-associated kinases in response to cytokines and growth factors, including IFNs, EGF, IL5, IL6, HGF, LIF and BMP2. The STAT4 protein product mediates responses to IL12 in lymphocytes, and regulates the differentiation of T helper cells.
References in periodicals archive ?
El Sharkawy added, "We found that patients with the risk genetic variation had lower expression of STAT4 in their liver and immune cells, reducing their immune response against hepatitis B and their production of interferon gamma, a protein responsible for moderating fibrosis."
Rezaei, "Association of stat4 gene single nucleotide polymorphisms with iranian juvenile-onset systemic lupus erythematosus patients," The Turkish Journal of Pediatrics, vol.
PSA: polysaccharide A; ASF: altered Schaedler flora; SCFA: short-chain fatty acids; SFB: segmented filamentous bacteria; APCS: antigen-presenting cells; TLR: Toll-like receptor; TH0, 1, 2, and 17 cells: T helper 0, 1,2, and 17 cells; Treg: regulatory T cell; SAA: serum amyloid A; MAPK: mitogen-activated protein kinase; JNK: c-Jun N-terminal kinase; ERK: extracellular signal-regulated kinase; NF-[kappa]B: nuclear factor kappa B; STAT4 and 6: signal transducer and activator of transcription 4 and 6; MHC: major histocompatibility complex; eNOS: endothelial nitric oxide synthase; VEGFR2: vascular endothelial growth factor receptor 2; Jak: Janus kinase; Tyk: tyrosine kinase; CREB: cAMP-response element binding protein; CRTC2: CREB-regulated transcription coactivator 2.
And also, the IL-12R01 and STAT4 protein expression significantly decreased (Figure 7(b)).
Marquez et al., "Association of the STAT4 gene with increased susceptibility for some immune-mediated diseases," Arthritis & Rheumatism, vol.
Caption: Figure 4: Potential binding sites for transcription factors of 1R, 2R, and 3R tandem repeat elements of the XRCC5 VNTR: XBP-1 =X-box binding protein 1; TFII-I = transcription factor II-I; STAT4 = signal transducer and activator of transcription 4; c- Ets-1 = c-E-twenty-six-1; E2F-1=E2F transcription factor 1; GR-beta = glucocorticoid receptor-beta; GCF = GC factor; NF-kappaB = nuclear factor- kappaB; RelA = v-rel avian reticuloendotheliosis viral oncogene homolog A.
Both undifferentiated mADSCs and cADSCs expressed [beta]-catenin, [beta]-catenin pS45, Akt (pS473), and Stat4 phosphorylation and only mADSCs expressed Stat5 phosphorylation.
IL-12 activates a series of phosphorylation events which permit STAT4 molecules to dimerize and translocate to the nucleus, upregulating a proinflammatory cascade.
They can also directly interact with gene expression factors and cell signaling involved in cytokine secretion, such as activator protein 1 (AP-1) [37] and signal transducer and activator of transcription 4 (STAT4) [38].
STAT1, STAT2, STAT3, STAT4, STAT5, and STAT6 are the main members of the STAT family [12, 13].
Various genes have been demonstrated to be relevant to different types of uveitis, comprising HLA-B27, HLA-A29, HLA-B51, HLA-DR4, IL-10, STaT4, STAT3, and UBAC2 [4-6] which suggested genetic factors are involved in the occurrence and development of uveitis.
During the course of these studies, >50 commonly occurring single-nucleotide polymorphisms (SNPs) were found to be associated with SLE, including human leukocyte antigen (HLA) regions HLA-DRB1-HLA-DQA1,[sup][5] HLA-DQB1-HLA-DQA2,[sup][6] and HLA-DQB2,[sup][6] as well as non-HLA genes (RasGRP3,[sup][5] STAT4,[sup][7] IRF5-TNPO3,[sup][5] ETS1,[sup][8] IKZF1,[sup][5] and TNFAIP3[sup][7]).