SOCS2

Last update 08 May 2025

Basic Info

Synonyms

CIS-2, CIS2, Cish2

+ [8]

Introduction

Substrate-recognition component of a cullin-5-RING E3 ubiquitin-protein ligase complex (ECS complex, also named CRL5 complex), which mediates the ubiquitination and subsequent proteasomal degradation of target proteins, such as EPOR and GHR (PubMed:11781573, PubMed:21980433, PubMed:25505247, PubMed:31182716, PubMed:34857742). Specifically recognizes and binds phosphorylated proteins via its SH2 domain, promoting their ubiquitination (PubMed:21980433, PubMed:25505247, PubMed:31182716, PubMed:34857742, PubMed:37816714). The ECS(SOCS2) complex acts as a key regulator of growth hormone receptor (GHR) levels by mediating ubiquitination and degradation of GHR, following GHR phosphorylation by JAK2 (PubMed:21980433, PubMed:25505247, PubMed:34857742). The ECS(SOCS2) also catalyzes ubiquitination and degradation of JAK2-phosphorylated EPOR (PubMed:11781573).

100 Clinical Results associated with SOCS2

100 Translational Medicine associated with SOCS2

0 Patents (Medical) associated with SOCS2

820

Literatures (Medical) associated with SOCS2

01 Jun 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Modified expression of JAK-STAT pathway genes in an in vivo rheumatoid arthritis model: A preclinical study to explore genetic insights

Article

Author: Siddiqui, Nadir Naveed ; Zehra, Sitwat ; Ghouri, Maham ; Ghauri, Humaira ; Avesi, Lubna ; Khan, Rizma ; Asif, Ehtisham ; Lateef, Mehreen

BACKGROUNDRheumatoid arthritis (RA) is a chronic inflammatory disease characterised by inflammatory synovial tissue, joint deterioration, and effects on systems other than the joints. The biological process underlying the progression of the disease remains unknown, however cell-mediated immunity plays an important part in the onset of RA. The current study investigated the involvement of the JAK-STAT pathway genes (JAK-1, IL-6, and SOCS-2) in the pathogenesis of RA (Rheumatoid arthritis).METHODOLOGYThe study was carried out on thirty male Albino Wistar rats categorised in to the three groups. The AIA (Adjuvant induced animal) model was utilised to study the disease pathogenesis. The haematoxylin and Eosin (H and E) was performed followed by ELISA and expression analyses by RT-q-PCR. The obtained data was analysed using one-way ANOVA (Analysis of Variance).RESULTSHistopathology confirmed that diseased group appeared to be severely impaired, demonstrating manifestations of inflammation with chronic as well as cartilage degenerative changes. Furthermore, chronic inflammation was also noticed in the intertrabecular area. The significant increased levels of JAK1, IL-6 and TYK-2 were recorded among RA group. The gene expression assessment indicated that higher expression of JAK-1 and IL-6 was linked to the further development of RA in the disease group. The SOSC2 (a negative regulator of the JAK-STAT pathway) was significantly (p < 0.01) downregulated. Moreover, SOCS2 may be unable to suppress the transcription of the related JAKs (IL-6 and JAK-1), resulting in the constant release of immune mediators and contributing to the pathophysiology of RA.CONCLUSIONSThe JAK-STAT pathway may serve as the target for diagnosing and treating inflammatory and autoimmune disorders (RA). The findings may enhance therapeutic possibilities by investigating the possible implications of JAK-STAT pathway genes as candidates for progressive rheumatoid arthritis therapies.

01 May 2025·Molecular Biotechnology

CEBPA Restrains the Malignant Progression of Breast Cancer by Prompting the Transcription of SOCS2

Article

Author: Chen, Deng-Feng ; Liu, Zhen ; Wang, Jin-Li ; Huang, Ao-Li ; Ji, Wei-Wei

The suppressor of cytokine signaling 2 (SOCS2) has been identified to act as a tumor suppressor in breast cancer (BC) progression. However, the action of SOCS2 in macrophage polarization in BC cells has not been reported yet. The qRT-PCR and western blotting were adopted for detecting the levels of mRNAs and proteins. The macrophage M2 polarization was analyzed by flow cytometry. Analyses of cell oncogenic phenotypes and tumor growth were conducted using 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, scratch, Transwell, tube formation assays in vitro, and tumor xenograft assay in vivo, respectively. The interaction between CEBPA (CCAAT Enhancer Binding Protein Alpha) and SOCS2 was confirmed using bioinformatics analysis and dual-luciferase reporter assay. SOCS2 was lowly expressed in BC tissues and cells. Functionally, overexpression of SOCS2 inhibited macrophage M2 polarization, and impaired BC cell proliferation, angiogenesis, and metastasis. Mechanistically, CEBPA bound to the promoter region of SOCS2, and promoted its transcription. A low CEBPA expression was observed in BC tissues and cells. Forced expression of CEBPA also suppressed macrophage M2 polarization, BC cell proliferation, angiogenesis, and metastasis. Moreover, the anticancer effects mediated by CEBPA were abolished by SOCS2 knockdown. In addition, CEBPA overexpression impeded BC growth in nude mice by regulating SOCS2. CEBPA suppressed macrophage M2 polarization, BC cell proliferation, angiogenesis, and metastasis by promoting SOCS2 transcription in a targeted manner.

24 Apr 2025·Nature

Comparative characterization of human accelerated regions in neurons

Article

Author: Hu, Ming ; Abnousi, Armen ; Cai, Charles ; Liu, Hongjiang ; Pollen, Alex A ; Keough, Kathleen C ; Pollard, Katherine S ; Fair, Tyler ; Amador, Zachary ; Beaman, Cooper ; Jones, Ian R ; Yang, Xiaoyu ; Cui, Xiekui ; Zhang, Meng ; Yang, Han ; Ye, Zhen ; Mishra, Shreya ; Shen, Yin ; Ren, Xingjie

Human accelerated regions (HARs) are conserved genomic loci that have experienced rapid nucleotide substitutions following the divergence from chimpanzees^1,2. HARs are enriched in candidate regulatory regions near neurodevelopmental genes, suggesting their roles in gene regulation³. However, their target genes and functional contributions to human brain development remain largely uncharacterized. Here we elucidate the cis-regulatory functions of HARs in human and chimpanzee induced pluripotent stem (iPS) cell-induced excitatory neurons. Using genomic⁴ and chromatin looping information, we prioritized 20 HARs and their chimpanzee orthologues for functional characterization via single-cell CRISPR interference, and demonstrated their species-specific gene regulatory functions. Our findings reveal diverse functional outcomes of HAR-mediated cis-regulation in human neurons, including attenuated NPAS3 expression by altering the binding affinities of multiple transcription factors in HAR202 and maintaining iPS cell pluripotency and neuronal differentiation capacities through the upregulation of PUM2 by 2xHAR.319. Finally, we used prime editing to demonstrate differential enhancer activity caused by several HAR26;2xHAR.178 variants. In particular, we link one variant in HAR26;2xHAR.178 to elevated SOCS2 expression and increased neurite outgrowth in human neurons. Thus, our study sheds new light on the endogenous gene regulatory functions of HARs and their potential contribution to human brain evolution.

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