SOCS3
- Known as:
- SOCS3
- Catalog number:
- 11-406-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- SOCS3
Related genes to: SOCS3
- 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
Related articles to: SOCS3
- In this Bioinformatics study, we took in account the cell types variation of tumor microenvironment (TME) in Pancreatic Ductal Adenocarcinoma (PDAC), with a particular attention to miRNAs dysregulated pathways influencing immune responses, and especially memory CD4+ T cells. - Source: PubMed
Publication date: 2026/05/22
Al-Janaby Mohammed SalihMannoush Salah HAl-Janabi Saif SSuleiman Ahmed AbdulJabbarAbdulkareem Ali HazimAlalwani Anmar KamilFahad Mustafa M - Neuroinflammation, driven by microglia activation and the production of pro-inflammatory cytokines, has been implicated in several neurological diseases and neuropathic pain. MicroRNAs (miRNAs) have emerged as important regulators of neuroinflammatory processes. Prior studies identified elevated levels of circulating miR-19a and miR-19b in individuals living with chronic pain following spinal cord injury (SCI). In this study, we wanted to determine whether miR-19a and miR-19b have a direct effect on microglia activation, specifically pro-inflammatory activation, associated with neuroinflammation. Microglia were activated by inflammatory stimuli in the presence of miR-19a or miR-19b mimics, and assessed for the expression of cytokines, chemokines, and effector molecules. The results show that miR-19a or miR-19b mimics increased the expression of pro-inflammatory cytokines, chemokines, and effector molecules in microglia. The results also showed decreased expression of suppressor of cytokine signaling (SOCS) proteins, namely SOCS1 and SOCS3, in activated microglia with miR-19a and miR-19b mimics. Additionally, enhanced signaling through the NFκB and Jak pathways was observed with increased NFkB-p65 and JAK1 phosphorylation in the presence of miR-19a and miR-19b mimics. Further results show that miR-19a and miR-19b inhibitors reversed these effects on activated microglia. Overall, our results demonstrate that miR-19a or miR-19b increased the expression of pro-inflammatory cytokines, chemokines, and effector molecules in activated microglia. These results indicate that miR-19a and miR-19b can enhance microglia activation and associated inflammatory responses, which may have implications for conditions associated with neuroinflammation. - Source: PubMed
Sahebdel FaezehBattaglino Ricardo AMorse Leslie ROlson Julie K - Atopic dermatitis (AD) is characterized by complex immune dysregulation primarily studied in lesional skin. Identifying circulating molecular signatures that mirror cutaneous inflammation could enable non-invasive disease monitoring. - Source: PubMed
Publication date: 2026/06/09
Fernández-Bernaldez AlbertoJiménez-Sánchez AnaChicharro PabloGonzález-Agudo CeliaSánchez-Cabo FátimaVara AliciaLlamas-Velasco MarGómez Manuel Joséde la Fuente Hortensia - Multiparity increases the risk of obesity in both humans and animal models. We have previously discovered an increase in proinflammatory cytokine mRNA levels in adipose tissues, placentas, and livers of females in their fourth vs first pregnancy, regardless of age or adiposity, suggesting an increased inflammatory state with subsequent pregnancies. The goal of the current study was to determine whether similar changes in inflammatory markers would be evident in the maternal brain in a fourth pregnancy compared to a first pregnancy, either at baseline or in response to an immune challenge. Females were studied at pregnancy 18.5 days post-conception (dpc; P), at 25 days postpartum (dpp; PP), and in age-matched never pregnant (NP) mice. Pregnant multiparous females had increased fat masses compared to females in their first pregnancy, and increased mRNA levels of Il6, Il1β, and Tnfα in the retroperitoneal and ovarian adipose tissue depots. While mRNA levels of hypothalamic proinflammatory genes were mostly similar in females at baseline, regardless of first vs fourth pregnancy or pregnancy status, LPS markedly induced inflammation in NP and PP females compared to P females; genes affected included Cxcl10, Ccl2, Il1β, Il6, Tnfα, Socs3, Nfkb, Tlr2, and Tgfβ. The response of Cxcl10, Socs3, and Tlr2 to LPS was greater in NP than PP females. Unlike the proinflammatory genes, a few noninflammatory genes had an age effect (mainly decreased with age), but not a pregnancy effect, including Dlg4, Dnmt1/3, Esr1, and Ki67. Overall, pregnant females were protected from a proinflammatory insult compared to NP and PP females. - Source: PubMed
Publication date: 2026/06/16
Laaker Collin JRebholz Sandra LWoollett Laura AReyes Teresa M - Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies worldwide, and diabetes mellitus has been recognized as both a risk factor for and a potential consequence of PDAC. However, the epidemiological trends and shared molecular mechanisms underlying this association are not completely understood. - Source: PubMed
Publication date: 2026/05/25
Zhang JiaxiLiu ZhibinHuang KeYi JunkooKim Myoung Ok