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The expression levels of phosphorylated STAT1 (p-[Ser.sup.727]), STAT3 (p-[Ser.sup.727]), and JAK2 (p- [Tyr.sup.1007]/[Tyr.sup.1008]8) molecules and un-phosphorylated (STAT1/3, JAK2, TYK2, and SOCS1) molecules in response to LILRB1 and LILRB3 gene-transfected HD11 cell line compared to mock control by western blotting were increased, and also significantly upregulated in STAT1/3, JAK2, TYK2, and SOCS1 mRNA by qRT-PCR.
The JAK-STAT1 pathway is activated by IFN-[gamma], and SOCS1 and SOCS3 are induced.
SOCS1 and SOCS3 inhibition in the latter study increased insulin sensitivity, decreased SREBP-1c to normal levels, and ameliorated fatty liver and hypertriglyceridemia dramatically in obese diabetic mice.
Role of SOCS1 in tumor progression and therapeutic application.
SOCS2 and CIS form a second group of related proteins that are more ubiquitously expressed than SOCS1 and SOCS3 but are relatively poor inhibitors of the actions of most cytokines.
Results: No disease-specific CpG island methylation of SOCS1 was observed.
The researchers say they were surprised to find that SOCS1 is linked to p53, the master regulator of natural anticancer defenses.
Constitutively elevated levels of SOCS1 suppress innate responses in DF-1 immortalised chicken fibroblast cells.
Other studies have also demonstrated that elevated miR-155 promotes foam cell formation and atherosclerosis by repressing its downstream target genes, including Bcl-6, SOCS1, HMG box-transcription protein 1 (HBP1), and mitogen-activated protein kinase 10 (MAP3K10) [16-19].
Different up-regulated proteins during the disease include insulin growth factor (IGF) II, a disintegrin and metalloproteases (ADAM) 9, signal transducers and activators of transcription (STAT) 3, suppressors of cytokine signalling (SOCS) 3, and cyclin D1 while the down-regulated proteins during the disease include collagen I, SMAD 4, fragile histidine triad (FHIT), and SOCS1.17 Other proteins include, POU class 5 homeobox 1 (OCT4), baculoviral IAP repeat containing 5 (BIRC5), cyclin D1 (CCND1), ATP binding cassette subfamily G member 2 (BCRP), SRY-box 2 (Sox2), Glutathione S-transferases (GST), NCK adaptor protein 1 (NCK1), human leukocyte antigen DQ (HLA-DQ), miR-106b, c-Myc, Ki67 and selective internal radiation therapy (SIRT).
Perez et al., "miR-150 promotes renal fibrosis in lupus nephritis by downregulating SOCS1," Journal of the American Society of Nephrology, vol.
Some evidences from Pan-HDAC inhibitors indicated that promoter-associated histone acetylation of SOCS1 and SOCS3 caused by HDACi may further downregulated JAK2/STAT3 signaling .
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