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)  and signal transducer and activator of transcription 4 (STAT4
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] HLA-DQB1-HLA-DQA2,[sup] and HLA-DQB2,[sup] as well as non-HLA genes (RasGRP3,[sup] STAT4
,[sup] IRF5-TNPO3,[sup] ETS1,[sup] IKZF1,[sup] and TNFAIP3[sup]).