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SOCS3Suppressor of Cytokine Signaling 3
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MicroRNA-19a-3p enhances the proliferation and insulin secretion, while it inhibits the apoptosis of pancreatic beta cells via the inhibition of SOCS3. Intl J Mol Med 2016; 38: 1515-1524, doi: 10.3892/ijmm.2016.2748.
(c) Western blotting of the markers of STAT3 signaling (p-STAT3, STAT3, and SOCS3), antiapoptosis (Bcl2 and Bcl-xl), and YAP in the liver in each group at 24 h and 48 h after PHx.
The top 15 hub genes, possessing high degree of connectivity in DCM, are as follows: IL6, MYC, ACTA2, SERPINE1, ASPN, SPP1, KIT, TFRC, FMOD, PDE5A, MYH6, FPR1, C3, CDKN1A, and SOCS3. Among these 15 hub genes, IL6, MYC, SERPINE1, SPP1, TFRC, MYH6, FPR1, C3, CDKN1A, and SOCS3 were significantly downregulated while ACTA2, ASPN, KIT, FMOD, and PDE5A were upregulated.
Three differentially expressed genes from E2- or ER agonist-treated cells identified by RNA-Seq, peroxisome proliferator-activated receptor gamma (PPARG, GeneID 5468), suppressor of cytokine signaling 3 (SOCS3, GeneID 9021), and interleukin 6 receptor (IL6R, GeneID 3570) were validated using quantitative PCR.
El Kochairi et al., "Activation of peroxisome proliferator--activated receptor-[beta]/[delta] (PPAR[beta]/[delta]) ameliorates insulin signaling and reduces SOCS3 levels by inhibiting STAT3 in interleukin-6-stimulated adipocytes," Diabetes, vol.
Conversely, SOCS3 plays a crucial role in inhibition of M1-like polarization in the downstream regulation pathway [55, 63].
The results indicated that pretreatment with Lactobacillus plantarum significantly prolonged survival, and the intracellular mechanism may be related to suppress the expression of SOCS3 (suppressor of cytokine stimulation-3) and increase the production of TNF-a and IL-10 [41].
Indeed, STAT1 is activated by an intracytoplasmic pathway activated by the transmembrane receptor of IFNy [9,10] and can be blocked by SOCS3, which play an important role in the regulation of this pathway [11,12].
Stambas, "Inhibition of reactive oxygen species production ameliorates inflammation induced by influenza A viruses via upregulation of SOCS1 and SOCS3," Journal of Virology, vol.
RT-PCR analysis showed that SOCS3 mRNA in JAR cells was inhibited successfully by 70% (Figure 8), and Western blot analysis showed that SOCS3 protein expression in JAR cells was silenced.