Ask about this productRelated genes to: SOCS3 antibody
- Gene:
- SOCS3 NIH gene
- Name:
- suppressor of cytokine signaling 3
- Previous symbol:
- -
- Synonyms:
- SSI-3, CIS3, SOCS-3, Cish3
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-13
- Date modifiied:
- 2019-04-23
Related products to: SOCS3 antibody
Related articles to: SOCS3 antibody
- Long COVID is characterized by persistent symptoms following acute SARS-CoV-2 infection, yet its biological mechanisms remain incompletely understood. Emerging evidence suggests that immune dysregulation, mitochondrial dysfunction, and altered cell survival pathways may contribute to prolonged symptomatology. In this cross-sectional study, peripheral blood mononuclear cells were collected from individuals with Long COVID approximately 10 months post-infection and from recovered individuals without Long COVID symptoms. Symptom burden was assessed using a composite domain-based score. mRNA expression of immune and antiviral genes (IL-6, IL-1β, IL-10, SOCS3, HIF-1α, OAS1, MAVS, IFN-α, IFN-γ), anti-apoptotic markers (MCL1, BCL-2, XIAP, LIVIN), cell cycle kinases (CDK4, CDK6), mitochondrial biogenesis and dynamics markers (NRF1, TFAM, PGC-1α, DRP1, MFN1/2, OPA1), and mitophagy regulators (PARKIN, PINK1) were quantified using quantitative real-time PCR. Data was analyzed by SPSS and GraphPad Prism. Individuals with Long COVID demonstrated significantly higher expressions of IL-6, IL-1β, IL-10, SOCS3, HIF-1α, OAS1, MAVS, NRF1, DRP1, PARKIN, MCL1, and LIVIN compared with recovered controls after using the Benjamini-Hochberg False Discovery Rate (FDR) method. Several transcriptional markers, particularly HIF-1α, IL-1β, IL-10, and NRF1, remained independently associated with symptom burden after adjustment for age and sex. Correlation analysis demonstrated coordinated transcriptional co-expression patterns across immune, antiviral, mitochondrial, and apoptosis-related genes. Long COVID at 10 months post-infection is associated with coordinated transcriptional alterations across multiple biological pathways. The association of these changes with symptom burden suggests a potential link between persistent immunometabolic activation and clinical manifestations. These findings are exploratory and highlight the need for longitudinal and functional studies to further elucidate underlying mechanisms. - Source: PubMed
Publication date: 2026/05/15
Ali Yumna HamidAbbas UzairKhalid Muhib UllahAhmed IshfaqueHussain NiazBaloch IsrarMahboob HaniahZafar Ali AhsanMusawwir Usama Abdul - Exploring the targeted regulatory effect of isorhynchophylline on lipopolysaccharide (LPS)-induced acute lung injury (ALI) by constructing a drug delivery system of GEF-modified exosomes derived from M2 macrophages (M2-Exos) loaded with isorhynchophylline (GEF-M2-Exos-IRN; GMI). - Source: PubMed
Publication date: 2026/05/14
Zou Jin-RuYang DanZhang Chuan-MingZhang LuZhang Hao-NanSong MiaoMa Jun-BingYang ZhengQiu Min - Radiotherapy (RT) resistance in glioma is closely linked to abnormal JAK/STAT signaling, but its upstream drivers are unclear. This study investigates the role of lysyl oxidase-like 4 (LOXL4) in this process. - Source: PubMed
Publication date: 2026/05/14
Du GuoDing ZhaojunHou JianxunSu QiuyuLi QinhongXia XiaohuiYang Zhao - Hydrogen sulfide (HS) has been reported to exert both protumor and antitumor functions. It is worthy to clarify the condition under which HS exerts antitumor effects and its underlying mechanism. Our previous study connected the immune checkpoint indoleamine 2,3-dioxygenase 1 (IDO1) and HS by revealing that HS downregulates IDO1 expression, leading to our hypothesis that antitumor effect of HS is associated with IDO1 expression in tumor cells. - Source: PubMed
Publication date: 2026/05/13
He Zhen Ning TonyMeng FangzhouQian XiaoyangLiu YuyingFang XinYang DanYang Qing - Avian influenza virus is a globally prevalent pathogen in poultry populations, causing severe economic losses to the poultry industry worldwide. In the present study, we demonstrate that miR-449c generates two mature isoforms including miR-449c-3p and miR-449c-5p and exerts potent inhibitory effects on avian influenza virus replication. Mechanistically, we identified distinct antiviral pathways mediated by these two mature miR-449c isoforms. MiR-449c-5p enhances type I interferon responses by targeting the Suppressor of cytokine signaling 3 (SOCS3), thereby suppressing avian influenza virus replication. Meanwhile, miR-449c-3p inhibits viral replication through direct targeting and binding to the PB1 gene of avian influenza virus. Furthermore, we characterized the role of avian SOCS3 in avian influenza virus infection. We found that SOCS3 promotes avian influenza virus replication by dampening interferon responses, which is achieved through its interaction with and subsequent degradation of interferon regulatory factor 7 (IRF7), a key transcription factor that drives the expression of interferon stimulated genes (ISGs). Collectively, our findings uncover a novel dual-mode antiviral mechanism orchestrated by avian miR-449c, providing a theoretical foundation for the development of novel antiviral strategies. - Source: PubMed
Publication date: 2026/05/12
Liu ZhiyuanFan MengluZheng YiqingZeng YiranHou ChenglinPing JiHui