Human Polyclonal SOCS3 Ab
- Known as:
- Human Polyclonal SOCS3 Antibody
- Catalog number:
- a0769
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal SOCS3
Related genes to: Human Polyclonal SOCS3 Ab
- 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: Human Polyclonal SOCS3 Ab
Related articles to: Human Polyclonal SOCS3 Ab
- Gastric ulcer (GU), characterized by complex and multifactorial etiology, remains a prevalent gastrointestinal disease globally. The traditional Chinese medicine Astragalus membranaceus (Fisch.) Bunge is recorded in numerous ancient books such as "Shennong Bencao Jing", "Bencao Gangmu", "Yao Lei Fa Xiang", and "Zhenzhu Nang" to have the functions of tonifying qi, strengthening the spleen, harmonizing the stomach, and promoting ulcer healing. Astragalus membranaceus, a classical Chinese medicinal plant embodying the concept of "medicine-food homology," prominently features astragaloside IV (AS-IV) among its active pharmacological constituents. Accumulating evidence suggests AS-IV confers gastroprotective benefits in various experimental gastric injury models through mechanisms likely involving antioxidant, and anti-apoptotic effects. However, the specific molecular nodes through which AS-IV modulates its gastroprotective effects have not been fully defined. - Source: PubMed
Publication date: 2026/07/15
Wang ShuoFeng Ya-SongZhang Ya-KunWang Shao-Xian - Adipocyte differentiation is central to adipose tissue development, yet the regulatory mechanisms and transcriptional networks remain incompletely understood. Here, we demonstrate that suppressor of cytokine signaling 3 (SOCS3) plays a pivotal role in regulating avian adipogenesis by modulating adipogenic transcriptional programs. Multiplex immunofluorescence revealed that SOCS3 is enriched in PDGFRα preadipocytes within abdominal fat but declines during late differentiation. Functional studies in primary adipocytes and ICP1 cell line showed that SOCS3 knockdown promotes, whereas overexpression inhibits, adipogenic differentiation. Transcriptomic profiling indicated that SOCS3 depletion remodels the adipogenic transcriptional landscape, upregulating adipogenic and metabolic genes while downregulating transcriptional inhibitors. Mechanistically, proteomic analyses and co-immunoprecipitation identified poly(ADP-ribose) polymerase 1 (PARP1) as a SOCS3-binding partner. SOCS3 stabilizes PARP1 by suppressing its ubiquitination, leading to increased PAR levels and inhibition of adipogenesis. PARP1 interacts with PPARγ and represses its transcriptional activity through a mechanism independent of enzymatic PARylation. Importantly, ligand activation of PPARγ weakens its interaction with PARP1 and alleviates PARP1-mediated repression of its transcriptional activity. Collectively, these findings reveal a previously unrecognized SOCS3/PARP1 axis that modulates the transcriptional programs driving chicken adipocyte differentiation, underscoring its critical role in adipogenesis. - Source: PubMed
Wang ZhengTian ZixuanQv LiuyingZhao MingyuZhao QiangsenMa ZhenhuaYue QiaoxianYin ZhongtaoHou ZhuochengLi Huifeng - Autophagy plays paradoxical roles in breast cancer, functioning as both a stress-adaptive survival mechanism and a tumor-suppressive process depending on cellular and microenvironmental context. However, the molecular logic governing this functional duality has remained incompletely understood. Emerging evidence identifies the Wnt/β-catenin-mTOR axis as a central signaling hub that integrates proliferative, metabolic, and developmental cues to determine the directionality and functional outcome of autophagy. Aberrant activation of Wnt/β-catenin signaling reinforces mTOR activity, suppresses autophagic flux, and promotes stemness, epithelial-mesenchymal transition, therapeutic resistance, and immune evasion. Conversely, inhibition of Wnt signaling can relieve mTOR-mediated autophagy repression, leading to context-dependent induction of cytotoxic or cytostatic autophagy. Beyond tumor cell-intrinsic effects, Wnt-mTOR-autophagy crosstalk critically shapes the tumor immune microenvironment. In particular, SOCS3 deficiency-driven activation of Wnt/mTOR signaling represses autophagy in early-stage myeloid-derived suppressor cells, thereby sustaining their survival and immunosuppressive function. This mechanism highlights autophagy as an immunometabolic fate switch that governs myeloid cell persistence and antitumor immune suppression. Importantly, autophagy also feeds back to restrain Wnt signaling through selective degradation of pathway components, establishing dynamic regulatory loops that fine-tune oncogenic signaling output. In this review, we synthesize current evidence to delineate the bidirectional crosstalk between Wnt/β-catenin signaling, mTOR activity, and autophagy in breast cancer. We discuss how this integrated network governs tumor cell states, immune suppression, and therapeutic responsiveness, and propose a biomarker-driven, context-specific framework for autophagy modulation. By integrating signaling, autophagy flux, and myeloid immune status, precision targeting of the Wnt-mTOR-autophagy axis may offer new opportunities to overcome therapeutic resistance and improve clinical outcomes in breast cancer. - Source: PubMed
Publication date: 2026/06/30
Zhang JianLiu ChuqinZhang Yunjian - Obesity exhibits pronounced sex-dependent differences in susceptibility and progression; however, the molecular mechanisms coordinating central energy sensing with peripheral thermogenic responses remain incompletely defined. Selenoprotein F (SELENOF), an endoplasmic reticulum (ER)-resident member of the selenoprotein family involved in protein quality control and redox-sensitive metabolic regulation, has not previously been investigated in the context of diet-induced obesity. In the present study, WT and SELENOF-deficient mice subjected to a 16-week high-fat diet (HFD) were combined with primary brown adipocyte experiments to determine the role of SELENOF in systemic metabolic homeostasis. SELENOF deficiency markedly aggravated HFD-induced weight gain, adipose tissue expansion, dyslipidemia, and hyperleptinemia selectively in female mice, whereas no genotype-dependent effects were observed in males. Mechanistically, SELENOF deficiency intensified hypothalamic ER stress and leptin resistance, as reflected by increased GRP78, p-IRE1α, and p-PERK expression together with SOCS3 upregulation, reduced STAT3 phosphorylation, and activation of the IKK/NF-κB inflammatory pathway. In parallel, SELENOF deficiency reduced circulating free triiodothyronine (FT) levels and the ratio of free triiodothyronine to free thyroxine (FT/FT ratio), and suppressed DIO2 and UCP1 expression in brown adipose tissue (BAT). Experiments in primary brown adipocytes further showed that SELENOF deficiency did not disrupt proximal β3-adrenergic signaling but attenuated the downstream induction of DIO2 and UCP1. Collectively, these findings provide preliminary evidence that SELENOF is associated with sex-dependent metabolic adaptation during HFD-induced stress by linking hypothalamic proteostasis with the thyroid hormone-related thermogenic signaling program in BAT. - Source: PubMed
Publication date: 2026/06/26
Li ZimengZhao PengyuYang WanruLiu Hongmei - Early synaptic dysfunction is a hallmark of Alzheimer's disease (AD), yet the astrocytic mechanisms underlying these alterations remain poorly defined. Here, we identify astrocyte perisynaptic processes (PAPs) as subcellular hotspots of early translational dysregulation in AD. Soluble Aβ₁-₄₂ rapidly enhanced global and local protein synthesis in primary astrocytes. In 5.5-month-old APP/PS1-dE9 (APP) mice, translating ribosome affinity purification (TRAP) revealed widespread remodeling of the PAP translatome, while whole-astrocyte translation remained largely unchanged. Dysregulated mRNAs were linked to neuroinflammation, synaptic remodeling, and endoplasmic reticulum stress, and alterations emerged prior to amyloid plaque deposition. Among them, Serpina3n encoding α1-antichymotrypsin exhibited increased mRNA abundance in PAPs, uncovering spatially restricted translational control. Mechanistically, early Serpina3n upregulation was partially driven by JAK-STAT3 signaling, with preferential effects in astrocyte processes. These findings provide a conceptual advance by demonstrating that local translation in astrocyte PAPs is an early and compartment-specific mechanism that may contribute to synaptic dysfunction and disease initiation in AD. - Source: PubMed
Publication date: 2026/07/09
Avila-Gutierrez Katiade Sauvage María Ángeles CarrilloDepret NoémieOudart MarcThompson RobinAlvear-Perez RodrigoPoulot-Becq-Giraudon YiannisKozlowski EstherMonnet HeloïseMailly PhilippeGarcia ValentinJourdren LaurentLucas AlexandreBemelmans AlexisHirbec HeleneEscartin CaroleCohen-Salmon Martine