SOCS1


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SOCS1

A gene on chromosome 16p13.13 that encodes a member of the suppressor of cytokine-signalling—i.e., STAT-induced STAT inhibitor—family, which are cytokine-inducible negative regulators of cytokine signalling. SOCS1 expression is induced by cytokines (e.g., IL2, IL3, erythropoietin, CSF2/GM-CSF and interferon-gamma), and it provides a negative feedback loop to attenuate cytokine signalling.
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The above observations that SOCS3 preferentially and competitively binds to the binding site of SH2-domain haematopoietic phosphatase (SHP2) on the gp130 and others regarding SOCS3 interaction with leptin receptor [112, 113] support the idea that the N-terminal domains of SOCS1 and SOCS3 are indeed functioning in a similar manner and that SOCS3 can act to inhibit JAK activation, but only when recruited to the appropriate site on an activated receptor [115].
The researchers also showed that the reintroduction of SOCS1 into tumour cells locked them into a permanent dormant state known as cell senescence preventing them from multiplying wildly as is typical of cancer cells.
These data showed that the level of SOCS1 protein, a target of miR-155, was lower at 6,12, and 24 h after ox-LDL exposure than at 0h (p <0.05).
SOCS family members, particularly SOCS1 and SOCS3, inhibit JAK/STAT signaling [29] through several mechanisms, including direct JAK inhibition, STAT binding, and targeting receptor complex and other signaling proteins for proteasomal degradation [30-32].
Wang, "Rheumatoid arthritis-associated microRNA-155 targets SOCS1 and upregulates TNF-[alpha] and IL-1[beta] in PBMCs," International Journal of Molecular Sciences, vol.
found high levels of IL-10 associated to reduce socs1 expression in DHF patients [27].
Furthermore, the decrease in inflammation-related genes such as Il-6, IL-10, and SOCS1 was observed.
In contrast to a previous study [50], we observed a decreased gene expression of the TLR modulatory factors SOCS1 and Tollip when PBMCs were stimulated in the presence of C4, which thus cannot explain the inhibitory effects on cytokine production.
(310) Differentially expressed genes in ALK+ ALCL included genes encoding classical ALCL markers (ALK, CD30, MUC1 or EMA), immunoregulatory cytokines (IL-26, IL-31RA, IL-9, IL-1R2), Th17 cell-associated molecules (IL-17A, IL-17-F, ROR[gamma]), proliferation associated molecules (CCNA1, AGT, PDE4DIP, UPK1B, CDC27), STAT3-regulated targets (SERPINB3, SERPINB4, SOCS1, SOCS3), genes identified in other tumors (RRAD, RAR[alpha], NRCAM, TMEM158, CA12), cytotoxic molecules (PRF1, GZMB), and immunosuppressive response molecules (LILRA3).
The 15 screened genes were chosen for (a) their demonstrated role in regulating cellular adhesion and their possible role in metastasis (TIMP3, CDH1, CDH13, and APC), or (b) their putative role in carcinogenesis (PPP1R13B, HSPA2, HSD17B4, ESR1, GSTP1, CYP1B1, BRCA1, MYOD1, SOCS1, TITF1, and GSTM3).
Targets of miR-155 are the suppressor of cytokine signaling 1 (SOCS1), CCAAT/enhancer-binding protein alpha (C/EBPa), and Smad2 [24, 36] which are important players in anti-inflammatory response.