SOCS1
- Known as:
- SOCS1
- Catalog number:
- PA1074
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- SDlabs
- Gene target:
- SOCS1
Related genes to: SOCS1
- Gene:
- SOCS1 NIH gene
- Name:
- suppressor of cytokine signaling 1
- Previous symbol:
- -
- Synonyms:
- SOCS-1, SSI-1, JAB, TIP3, Cish1
- Chromosome:
- 16p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-13
- Date modifiied:
- 2015-08-26
Related products to: SOCS1
anti-SOCS1anti-SOCS1 (C-Terminus)anti-SOCS1 (C-Terminus)anti-SOCS1 (C-Terminus)anti-SOCS1 (N-Terminus)anti-SOCS1 (N-Terminus)Anti-SOCS1 AntibodyAnti-SOCS1, Goat Polyclonal to SOCS1, Isotype , Host Goatanti-SOCS1, Rabbit polyclonal to SOCS1, Isotype IgG, Host Rabbitanti-SOCS1, Rabbit polyclonal to SOCS1, Isotype IgG, Host RabbitAntibodies: SOCS1 HOST: Goat Clonality: pAbCish1,JAB,JAK-binding protein,Mouse,Mus musculus,Socs1,SOCS-1,Ssi1,SSI-1,STAT-induced STAT inhibitor 1,Suppressor of cytokine signaling 1ELISA Kit FOR Suppressor of cytokine signaling 1; organism: Mouse; gene name: Socs1ELISA Kit FOR Suppressor of cytokine signaling 1; organism: Rat; gene name: Socs1ELISA Kit for Suppressors Of Cytokine Signaling 1 (SOCS1) Related articles to: SOCS1
- Myocardial fibrosis is a key pathological feature of heart failure (HF) linked to aberrant macrophage polarization. Although the traditional Chinese medicine Shenfu injection (SFI) clinically improves HF and has been found to inhibit M1 macrophage polarization and fibrosis, its mechanisms remain unclear. This study aimed to elucidate how SFI regulates macrophage-cardiac fibroblasts (CFs) communication - specifically via exosomal miR-155-5p from M1 macrophages. - Source: PubMed
Publication date: 2026/06/18
Wang FeiHu SiyuanLi LinLian KunZhang JunyuLi XinchunFang GeHu Zhixi - Stem cell-like memory T (Tscm) cells are long-lived, self-renewing T cells that sustain chronic immune activation. We analyzed Tscm cells from 11 rheumatoid arthritis (RA) patients and 8 healthy controls using single-cell RNA sequencing and proteomics, comparing csDMARD-treated, tofacitinib-treated, and control groups. RA CD4 Tscm cells exhibited a distinct signature with upregulation of STAT3 and downstream targets including MYC, PIM1, SOCS1, and SOCS3, while proteomic analysis of the bulk sorted Tscm population confirmed increased STAT3 and MYC-associated pathways in total Tscm cells. Although JAK inhibition partially attenuated this signaling, it did not fully suppress STAT3 activity. Notably, MYC target gene activity correlated with clinical disease severity. These findings indicate that elevated STAT3-MYC transcriptional signatures in RA CD4 Tscm cells may contribute to treatment resistance and suggest MYC-driven transcriptional reprogramming as a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/17
Yang SeojinKim MiriamPark Kyoung-LinKim HyunjiPark Jun WonPark Jin KyunLee Eun Bong - Japanese encephalitis virus (JEV) is a mosquito-borne zoonotic virus with pig as its major amplifying host. Despite that JEV can persistently infect the placentae of pregnant sows and cause severe reproductive failures, the molecular responses and potential regulators of JEV infection in pig placenta remain unclear. By using porcine trophectoderm (pTr) cells as model, we investigated the transcriptomic changes during JEV infection, with special focus on microRNA-centric regulation over immune genes and JEV infection. To avoid currently poor microRNA annotation for pig, we first performed small RNA-seq to achieve refined microRNA annotation, with hundreds of novel microRNAs annotated. After confirming that JEV can efficiently infect pTr cells and induce severe cytopathic effects, we conducted routine and small RNA-seq to determine the changes of mRNA and microRNA genes during JEV infection. We identified > 1000 differentially expressed genes and found JEV-induced genes are tightly associated with antiviral immune responses. Moreover, we identified 94 JEV-affected microRNAs, including many with their roles on viral infection still unclear. Focusing on JEV-affected microRNAs, we constructed a microRNA - mRNA negative regulatory network, with multiple hub microRNAs and their targets inspected. Among these microRNAs, we experimentally validated that ssc-miR-149 and ssc-miR-483 both can inhibit JEV replication in pTr cells, with the well-recognized immune suppressor SOCS1 validated as a direct target of ssc-miR-149. Overall, this study comprehensively characterized the microRNA-centric regulation of JEV infection in pTr cells, which provides mechanistical insights on JEV infection in pig placenta and will facilitate the development of novel therapies against JEV infection. - Source: PubMed
Publication date: 2026/06/17
Yang JuanJiang JiayaoGong JiajiaZhang LinjieLi ChenxiBao XiaochengFan HairuiDai ChaohuiLi YanhuaChen ShuaiSun Ming-A - Antisense oligonucleotides offer a powerful strategy for suppressing pro-inflammatory microRNAs, but efficient long-term delivery after systemic administration remains challenging. In this study, we developed a self-assembling oligoDNA-nanomicelle (OD-micelle) platform to simultaneously deliver antisense oligoDNA targeting miR-155 and curcumin, a hydrophobic anti-inflammatory agent, to the lung. The curcumin formulation (OD-micelle/Cur) can be administered intravenously and has a negatively charged surface and average particle size of ∼160 nm, supporting scavenger receptor (SR)-mediated pulmonary delivery. Fluorescence imaging and flow cytometry analyses demonstrated that cellular uptake was comparable to that of OD-micelle/PEI25k, a widely used cationic carrier standard. Hemocompatibility tests demonstrated reduced red blood cell aggregation, compared with PEI25k, indicating improved hemocompatibility without compromising delivery efficiency. Mechanistic studies supported the receptor-dependent transport of the oligoDNA corona. Pre-treatment with excess oligonucleotides reduced the cellular uptake and lung accumulation of Cy5-labeled OD-micelle/Cur. Furthermore, a RAGE antagonist peptide similarly reduced cellular uptake, suggesting the involvement of RAGE in the SR pathway. In LPS-induced acute lung injury (ALI) mice and LPS-stimulated Raw264.7 cells, the OD-micelle/Cur suppressed the inflammatory response, decreased TNF-α and IL-6 levels, and improved lung histopathology. The antisense oligoDNA corona contributed to the efficacy through miR-155 inhibition, which was confirmed by comparison with scrambled OD-micelle/Cur and increased SOCS1 expression in lung tissue. Furthermore, RAGE pathway inhibition attenuated the inflammatory response, suggesting that RAGE signaling could be an additional therapeutic mechanism. Therefore, OD-micelles are a systemically administrable, lung-targeted oligonucleotide nanoplatform with dual-mechanism anti-inflammatory activity for the treatment of ALI. - Source: PubMed
Publication date: 2026/05/29
Kang MinjiOh JihunKim EunjyLee Minhyung - The favorable prognosis of pediatric AML1::ETO acute myeloid leukemia (AML) is well-established, yet the impact of co-occurring KIT mutations-particularly in exon 17-on clinical outcomes and chemosensitivity remains incompletely defined. - Source: PubMed
Publication date: 2026/06/15
Hu ZhilinTang XueChen FenLi TonghuiLiu YiZhou GuichiLi QianLiu ShilinWang YingWen FeiqiuMai HuirongWang LuluLiu Sixi