SOCS3

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SOCS3

A gene on chromosome 17q25.3 that encodes a protein which interacts with multiple activated proteins of the tyrosine kinase signalling pathway, including IGF1 receptor, insulin receptor and JAK2.

Molecular pathology
SOCS3 is thought to be a susceptibility gene for atopic dermatitis.
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Keywords: Hypertension, Pregnancy, SOCS-3, Obesity.
In this way, SOCS is said to be involved in the regulation of the inflammatory mediators, controlling the degree of the adverse effect.6 Lately, additional roles are identified in suppressing the inflammatory pathways in the immune system and in cancer biology.7 Yet, the functional importance of SOCS-3 in regulating vascular health is largely unknown but may be taken as an upcoming marker for metabolic diseases8 (Figure-1A).
ELISA assays were used to detect SOCS-3 levels (kit cat # H1415 by Glorybioscince, Belgium).
Roberts and colleagues showed that mice with a deletion of SOCS-3 gene died at midgestation because of the placental defects.
In this study, we observed the effects of Kidney-replenishing herbs on the proliferation and apoptosis of human first-trimester trophoblasts; we therefore investigated the effects of the herbs on the expression of SOCS-3 in human trophoblasts by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot.
Rabbit anti-human SOCS-3 antibodies, mouse anti-phosphoERK monoclonal antibodies, rabbit anti-ERK monoclonal antibodies, and mouse anti-GAPDH were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).
There are seven SOCS family proteins: SOCS-1, SOCS-2, SOCS-3, SOCS-4, SOCS-5, SOCS-6, and SOCS-7, each of which has a central SH2 domain, an amino-terminal domain of variable length and sequence, and a carboxy-terminal 40-amino-acid module known as the SOCS box (Tamiya et al.
Renauld, "Interleukin 9 induces expression of three cytokine signal inhibitors: cytokine-inducible SH2-containing protein, suppressor of cytokine signalling (SOCS)-2 and SOCS-3, but only SOCS-3 overexpression suppresses interleukin 9 signalling," Biochemical Journal, vol.
El-Haschimi et al., "Activation of SOCS-3 messenger ribonucleic acid in the hypothalamus by ciliary neurotrophic factor," Endocrinology, vol.
In this context, "SOCS-3 silencing" might permit constitutive STAT 3 signalling.
Further investigations revealed that, at the molecular level, IL-7 switched off a gene called SOCS-3.
"In an overwhelming infection, SOCS-3 becomes highly activated and suppresses the immune response, probably as a natural precaution to prevent 'out-of-control' responses that cause collateral damage to body tissue," Pellegrini said.