Polyclonal Rabbit COPS2 Antibody
- Known as:
- Polyclonal Rabbit COPS2 Antibody
- Catalog number:
- KA0863
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit COPS2 Antibody
Ask about this productRelated genes to: Polyclonal Rabbit COPS2 Antibody
- Gene:
- COPS2 NIH gene
- Name:
- COP9 signalosome subunit 2
- Previous symbol:
- -
- Synonyms:
- TRIP15, ALIEN, CSN2
- Chromosome:
- 15q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-03
- Date modifiied:
- 2014-11-19
Related products to: Polyclonal Rabbit COPS2 Antibody
Related articles to: Polyclonal Rabbit COPS2 Antibody
- Keel length is a key body size indicator, which has an important impact on the overall growth performance, bone health, and production performance of poultry. In the process of selecting crossed strains for yellow feathered broiler chickens, it is generally necessary to select keel length, but there is little research on keel length development. Therefore, resequencing and GWAS was employed to obtain SNP molecular markers associated with keel length in a specialized Yellow-feathered broiler line. We identified 10 SNPs that were potentially significantly correlated with keel length for the first time located at 9 genes, including ATP7B, CST3, OTOP1, CRMP1, SLC12A1, COPS2, FAM227B, IFT140, APLP2. SNP2 and SNP3 loci were in a strongly linked state (D ' value=1), the other 8 SNP loci were not in a strongly linked state (D 'value<1). The association analysis between single SNP marker and keel length traits showed that TT and CT at SNP1 (rs315701680), GG at SNP2 (rs738740137), AA at SNP3 (rs317223723), AA at SNP4 (rs732443622), GG at SNP5(rs315667756), CC at SNP6 (rs314381113), GG at SNP7 (rs732811384), TT at SNP8 (rs314197610), CC and TC at SNP9 (rs13782000), TT and GT at SNP10 (rs737401141) genotypes were all the dominant genotypes for keel length. The strong linkage between SNP2 and SNP3 resulted in two haplotypes H1 (AG) and H2 (GA), respectively. The H1H1 haplotype (GGAA) produced by SNP2 and SNP3 linkage was the dominant genotype for keel length. The SNP molecular markers and dominant genotypes at SNP1-SNP10 loci identified in this study may be used to improve the accuracy and genetic progress of keel length selection. Meanwhile, candidate genes potentially significantly related to keel length will lay the foundation for genetic selection of keel length and cultivation of high-quality yellow feathered broilers in the future. - Source: PubMed
Publication date: 2026/03/27
Tu Y JLiu Y FZhang MJu X JShan Y JJi G GShu J T - Autophagy serves as a cellular defense against pathogens, while viruses exploit it through evolutionary arms races. Here, using Classical Swine Fever Virus (CSFV), an enveloped RNA pestivirus threatening global swine industries, we uncover a biphasic autophagy-hijacking strategy coordinated by COP9 signalosome subunit 2 (COPS2). Mechanistically, CSFV hijacks COPS2-mediated K11/K48-linked ubiquitination of viral P7 protein to create an autophagy recognition signal and facilitate virus entry into autophagosomes. In addition, COPS2 drives STX17-SNAP29-VAMP8 complex assembly by inhibiting SNAP29 O-GlcNAcylation, accelerating autophagosome-lysosome fusion to generate exocytosis-competent autolysosomes for viral release. This spatiotemporal regulation enables non-lytic viral propagation via autolysosomal exocytosis. Our study provides the first evidence that RNA viruses commandeer both ends of the autophagy machinery for complete replication cycles, identifying COPS2 as a master coordinator of autophagic flux hijacking and revealing the COPS2-SNAP29 axis as a conserved therapeutic target against enveloped RNA viruses. - Source: PubMed
Publication date: 2025/11/19
Wu KekeLi BingkeZhao RuiboBai YeZeng SenDing HongxingYi LinFan ShuangqiChen Jinding - Intervertebral disc degeneration (IVDD) is a primary cause of chronic low back pain, significantly impacting quality of life and healthcare systems globally. Despite its prevalence, the molecular mechanisms underlying IVDD remain unclear, and effective biomarkers are lacking. This study aims to identify circulating protein biomarkers causally linked to IVDD and explore their potential as biomarkers. - Source: PubMed
Publication date: 2025/07/31
Bai FanWang LingtingLiu HeHe YufeiWang Hong - Previous studies have demonstrated a close association between neddylation modifications and tumor progression as well as alterations in the microenvironment. This study aimed to explore the role of neddylation in bladder cancer (BLCA) progression and its prognostic significance. - Source: PubMed
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Xiaolong HuangMin DengSizhou ZhangDaorong HuJuncheng PanYanjian WangHong Li Jie GuJi ZhengQingjian Wu - Mucinous epithelial ovarian cancer (mEOC) is a rare subtype of epithelial ovarian cancer, characterized by poor responses to standard platinum-based chemotherapy. Polo-like kinase 1 (PLK1) is a key regulator of mitosis and cell cycle progression and its inhibition has been recently identified as a target in mEOC. In this study, we aimed to identify further therapeutic targets in mEOC using a CRISPR/Cas9 library targeting 3015 genes, with and without treatment with onvansertib, a PLK1 inhibitor. We identified twelve genes associated with cell survival (, , , , , , , , , , , and ) and three genes (, , and ) in synthetic lethality with onvansertib treatment. We validated that downregulation is important for the growth of mEOC cells through esiRNA interference and the use of a pharmacological inhibitor Momordin Ic. The downregulation of and combined with subtoxic doses of onvansertib interfered with mEOC cell growth. Interestingly, the combination of navitoclax, an inhibitor of BcL2 family members including BCL2L2, was synergistic in all four of the mEOC cell lines tested and substantially induced cell death through apoptosis. These data support the use of a combination of navitoclax and onvansertib as a new therapeutic strategy for mEOC. - Source: PubMed
Publication date: 2025/01/08
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