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
- Hypoxic-ischemic encephalopathy (HIE) is a severe neurological disorder with complex pathogenesis. The role of telomere-associated genes in HIE remains unclear. This study aims to investigate their alterations and mechanisms to provide new therapeutic insights. - Source: PubMed
Publication date: 2026/09/10
Chen HuaqingLu YanpingXiong DonglianZheng WenjuanXie Yi - To assess STAT3 activation in peri-implantitis tissues and to evaluate the STAT3-associated response of oral epithelial cells (OECs) to peri-implantitis-associated bacteria. - Source: PubMed
Publication date: 2026/09/09
Arce MarionEspinoza-Arrue JoaquinSansores-España DanielMorales MatiasFarfan Mauricio JSanz MarianoAbusleme LoretoDutzan Nicolas - Dysregulated macrophage polarization and persistent inflammation drive post-injury endometrial fibrosis and intrauterine adhesion (IUA), yet non-invasive early strategies remain limited. This study investigated the therapeutic effects and mechanisms of low-intensity pulsed ultrasound (LIPUS)-induced macrophage reprogramming in alleviating endometrial fibrosis and restoring fertility. - Source: PubMed
Publication date: 2026/09/03
Liang XiaowenGuo ZhiliLi MingjieDu MengHe YaohuiLian YixiangQiu WeibaoZhang ZenanYu HongChen Zhiyi - Loss-of-function mutations in DLK1, encoding Delta Like Non-Canonical Notch Ligand 1, have been linked to central precocious puberty (CPP) and increased body fat in girls, suggesting a role in the connection between metabolism and reproduction. DLK1 is located in the imprinted region of human chromosome 14, and mice lacking Dlk1 exhibit growth retardation and metabolic changes, phenotypes that overlap with Temple syndrome, an imprinting disorder associated with precocious puberty. However, the mechanisms by which DLK1 influences pubertal timing remain unclear. We investigated pubertal timing in Dlk1 knockout (KO) mice with either global or selective central nervous system (CNS) deletion of Dlk1, compared with control mice. Puberty onset and body weight were assessed, along with potential mediators of pubertal timing, including leptin and kisspeptin. Dlk1KO females reached puberty at the same age as controls, despite lower body weight. Dlk1KO males had delayed preputial separation but, like females, reached puberty at significantly lower body weight. Serum leptin and hypothalamic Socs3 mRNA, a downstream leptin effector, were lower peri-pubertally in Dlk1KO females than in controls. Kiss1 mRNA levels in the mediobasal hypothalamus were significantly lower in Dlk1KO females at puberty onset. Selective Dlk1 deletion in neurons and glial cells did not affect pubertal timing. These findings suggest that peripheral sources of Dlk1 contribute to the metabolic and endocrine regulation of pubertal timing. The absence of Dlk1 appears to alter the metabolic milieu in which puberty occurs, allowing activation of the reproductive axis despite low body weight and reduced hypothalamic kisspeptin expression. - Source: PubMed
Macedo Delanie BPereira Sidney AWang MeijiaoKyeol Han KimCarroll Rona SLatronico Ana ClaudiaAbreu Ana PaulaKaiser Ursula B - - Source: PubMed
Publication date: 2026/08/29
Ashmawy Ahmed IEl-Abhar Hanan SAbdallah Dalaal MAli Mennatallah A