Ask about this productRelated genes to: SOCS5 antibody
- Gene:
- SOCS5 NIH gene
- Name:
- suppressor of cytokine signaling 5
- Previous symbol:
- -
- Synonyms:
- KIAA0671, SOCS-5, CIS6, CISH6, Cish5
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-13
- Date modifiied:
- 2014-11-19
Related products to: SOCS5 antibody
Related articles to: SOCS5 antibody
- Eggshell quality is a critical trait in poultry production, as it directly influences economic outcomes. The genetic architecture underlying this trait remains poorly characterized. In this study, we conducted a genome-wide association study (GWAS) on Chinese Wenshang Barred chickens at 43 weeks of age to identify genomic loci and candidate genes associated with eggshell quality. This analysis revealed 87 significant SNPs and 14 candidate genes. Genes including , , , , and were associated with eggshell weight; , , , , and with eggshell thickness; and and with eggshell strength. Notably, three SNPs emerged as the most promising markers for eggshell quality, though their functional roles in laying hens require further investigation. This study advances our understanding of the genetic basis of eggshell quality and holds significant practical implications for improving this trait through targeted breeding strategies. - Source: PubMed
Publication date: 2026/07/11
Wang JieHan HaixiaLiu JieLei QiuxiaLiu WeiSun YanHao DanLi FuweiWang XinxiaCao DingguoZhao XinhuaZhou Yan - Colorectal cancer (CRC) is a highly prevalent malignancy with limited treatment options for advanced stages, and immune checkpoint blockade (ICB) efficacy is restricted by primary or acquired resistance. This study investigated the role of suppressor of cytokine signaling 5 (SOCS5) in CRC progression and immune evasion. We found SOCS5 is overexpressed in CRC tissues and correlates with poor patient prognosis. Functionally, SOCS5 does not affect CRC cell proliferation but impairs anti-tumor CD8 T-cell immunity by negatively regulating type I interferon (IFN-I) signaling. Mechanistically, SOCS5 acts as an E3 ubiquitin ligase to promote K48-linked ubiquitination and degradation of IFNAR1, inhibiting IFN-I pathway activation. Furthermore, high SOCS5 expression is associated with reduced ICB response in CRC patients, and targeting SOCS5 enhances the efficacy of anti-PD-1 therapy in preclinical models by boosting CD8 T-cell-mediated anti-tumor immunity. These findings identify SOCS5 as a novel prognostic biomarker and therapeutic target to improve ICB outcomes in CRC. - Source: PubMed
Publication date: 2026/07/14
Yu ChengpengDing YiLiang ShujingXiao ZitianWang ZeyuWan Dong - - Source: PubMed
Publication date: 2026/05/21
- To regulate immune and inflammatory responses, suppressor of cytokine signalling (SOCS) proteins bind to multiple signalling components downstream of cytokine receptors, such as Janus kinase (JAK) and signal transducers and activators of transcription (STAT). Dysfunctional SOCS proteins in immune and tissue-resident cells may contribute to chronic inflammation. Abnormal expression of SOCS proteins, including SOCS1, SOCS2, SOCS3, SOCS5, SOCS6, and SOCS7, has been reported in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), playing a vital role in disease pathogenesis. The expression of SOCS1 and SOCS3 varies across different cell types and stages of the disease. Genetic polymorphisms, epigenetic modifications, microRNAs, cytokines, hormones, therapeutic agents, and gender factors can influence SOCS1 and SOCS3 expression in MS patients and EAE mice. The functional impact of SOCS1 and SOCS3 is cell-type specific, with distinct roles in T cell subsets, microglia/macrophages, dendritic cells, astrocytes, and oligodendrocytes. In particular, SOCS1 and SOCS3 affect T cell subset differentiation, Th17/Treg cell balance, microglial/macrophage polarization, dendritic cell functions, as well as oligodendrocyte survival and activity. Therapeutic approaches targeting SOCS molecules, including SOCS1 mimetic peptides, have demonstrated promise in EAE models. This review provides a comprehensive explanation regarding the expression patterns of SOCS molecules in MS patients and EAE model, factors affecting their expression and their mechanistic role in disease immunopathogenesis, as well as highlights their potential as a therapeutic target for MS. - Source: PubMed
Jafarzadeh AbdollahMikaeili NargesJafarzadeh Zahra - BACKGROUND: Parkinson’s disease (PD) is the second most common neurodegenerative disorder worldwide, characterized by the loss of dopaminergic neurons in the substantia nigra. Recent studies suggest that immune dysregulation and alterations in signaling pathways play a key role in PD pathogenesis. The aim of this study was to investigate the expression of Signal transducer and activator of transcription (STAT) and Suppressor of cytokine signaling (SOCS) family genes in PD patients compared to control group. METHODS: Expression of STAT and SOCS family genes in peripheral blood cells were measured using RT-qPCR technique and the results were statistically analyzed using R software. RESULTS: There was no significant difference in the expression of STAT1, STAT3, STAT4, and STAT6 genes between the patient and control groups. However, the expression of SOCS1, SOCS2, SOCS3, SOCS5, and STAT5a genes in patients showed a significant decrease compared to the control group (p < 0.001, = 0.003, = 0.004, = 0.03 and = 0.007 respectively). Such decreases were significant between male subgroups for all these genes except SOCS5, for which neither male nor female subgroups showed a statistically significant difference. Regarding age, the expression of STAT1 and STAT6 genes decreased with increasing age (p = 0.046 and 0.04 respectively), while the decrease in STAT5a expression with increasing age was only seen in females (p = 0.001). CONCLUSION: Our study demonstrated that the expression of STAT5a, SOCS1, SOCS2, SOCS3, and SOCS5 genes was significantly reduced in PD. Given that these molecules play a crucial role in anti-inflammatory pathways, their reduced expression may indicate defect in these pathways that contribute to the pathogenesis of PD. However, further studies are required to elucidate the exact effects of these changes. - Source: PubMed
Publication date: 2026/04/25
Salmani MahyarRastegari-Pouyani MohsenAfshar SaeidTalebi-Ghane ElahehEftekharian Mohammad Mahdi