Ask about this productRelated genes to: ASB7 antibody
- Gene:
- ASB7 NIH gene
- Name:
- ankyrin repeat and SOCS box containing 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 15q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-05
- Date modifiied:
- 2015-08-24
Related products to: ASB7 antibody
Related articles to: ASB7 antibody
- Osteosarcoma is a highly heterogeneous and aggressive malignancy with a strong propensity for metastasis, highlighting the need to define its molecular drivers. Here, we report that ASB7 promotes tumor cell protrusion formation, invasion, migration, and lung metastasis. High expression of ASB7 is correlated with a poor prognosis. ASB7 forms an E3 ubiquitin ligase complex with CUL5 to ubiquitinate ATF2 at K383 and promote its proteasomal degradation. ATF2 reduction impairs HDAC6 recruitment to the ITGB2 promoter, thereby alleviating the transcriptional repression of ITGB2. Elevated ITGB2 expression subsequently promotes tumor lung metastasis. Our findings reveal that the ASB7-ATF2/HDAC6-ITGB2 axis regulates osteosarcoma metastasis and suggest potential treatment targets. - Source: PubMed
Publication date: 2026/05/05
Zou YeziZhong JianliangHuo LanqingChen JialiYu XinhaoWang JingxuanChen ZhenxuanYin LifengZeng CuilingZhang XiaHan ShanZhang RuhuaZhang Xing-DingKang TiebangZhou Liwen - Osteoarthritis (OA) is a degenerative joint disease with high global prevalence, and YKL-40 is an important factor related to the pathological process of OA. Increased levels of YKL-40 exert a protective influence against TNF-α-induced apoptosis in chondrocytes, thereby enhancing chondrocyte survival and activation, while counteracting TNF-α-driven expression of specific inflammatory mediators such as S100A8/A9.This study aims to evaluate the role and molecular mechanism of YKL-40 on chondrocytes in OA and provide a potential therapeutic avenue requiring further validation. A meta-analysis compared serum YKL-40 and TNF-α levels between OA patients and healthy controls. In vitro experiments examined the effects of YKL-40 on TNF-α-induced OA chondrocytes, assessing proliferation, differentiation, apoptosis, and inflammatory pathways. Meta-analysis revealed significantly elevated serum levels of YKL-40 and TNF-α in osteoarthritis (OA) patients compared to healthy controls. In vitro, TNF-α (10 ng/mL) induced extracellular matrix (ECM) degradation in chondrocytes, significantly reducing glycosaminoglycan (GAG) and type II collagen content. This degradation was effectively rescued by YKL-40 (100 ng/mL). RNA sequencing identified differentially expressed genes in TNF-α-treated chondrocytes, enriched in pathways like IL-17 and NF-κB signaling. YKL-40 treatment reversed the expression of key genes altered by TNF-α. Crucially, these differentially expressed genes (including S100A8/A9, ISG15, CDSN, BAAT, PTPN4, NPTX1, SMARCA1) were validated in independent OA cartilage and synovium GEO datasets. Protein-protein interaction (PPI) networks highlighted central genes within treatment groups. Western blotting confirmed YKL-40 counteracted TNF-α-induced NF-κB pathway activation (reduced p65 and IκBα phosphorylation) and modulated key targets (S100A8/A9, ASB7, ZFPM2), consistent with qRT-PCR data. YKL-40 is a promising biomarker and therapeutic target for OA. Its interplay with TNF-α provides a molecular basis for novel therapies targeting chondrocyte dysfunction, guiding future translational research. - Source: PubMed
Publication date: 2026/04/27
Li ZhuozhengSun XueXie YongfangHong ZexinDou ZeminYan ShichaoZhang YulongQin HeLiu DanFeng TingtingWang Guohui - - Source: PubMed
Publication date: 2025/11/14
Zhou XinyuHiggins Jonathan M GWang Fangwei - The maintenance of histone H3 lysine 9 trimethylation (H3K9me3) involves the recognition of preexisting modifications by heterochromatin protein 1 (HP1), which recruits the methyltransferase suppressor of variegation 3-9 homolog 1 (SUV39H1) to methylate the adjacent newly incorporated histones, establishing a positive feedback loop. However, how this positive feedback is restricted to maintain H3K9me3 homeostasis remains largely unknown. We performed an unbiased genome-scale CRISPR-Cas9 screen and identified CUL5 E3 ubiquitin ligase as a negative regulator of H3K9me3. ASB7 is recruited to heterochromatin by HP1 and promotes SUV39H1 degradation. During mitosis, cyclin-dependent kinase 1 (CDK1) phosphorylates ASB7, preventing its interaction with SUV39H1, leading to SUV39H1 stabilization and H3K9me3 restoration. Our findings reveal a dynamic circuit involving HP1, SUV39H1, and ASB7 that governs H3K9me3 homeostasis, ensuring faithful epigenetic inheritance and preventing excessive heterochromatin formation. - Source: PubMed
Publication date: 2025/05/29
Zhou LiwenChen ZhenxuanZou YeziZhang XiaWang ZifengZhu HongwenLin JiahuiHuang ZiyaoZheng LisiChen JialiXie MinerZhang MeifangZhang RuhuaZhu MingluWang ZiwenZhou HuGao SongYin YuxinWu YuanzhongKang Tiebang - Non- species (NHPH) are known to be present in the stomachs of humans and animals and are associated with their health. Here, we report complete genome sequences of type strains of , , and , which are major gastric NHPH species associated with human gastric diseases. - Source: PubMed
Publication date: 2025/05/20
Aoki SaeRimbara EmikoMatsui HidenoriKenri TsuyoshiSuzuki Masato