Hsp70B prime pAb
- Known as:
- Hsp70B prime pAb
- Catalog number:
- ASASPA-756E
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Hsp70B prime pAb
Related genes to: Hsp70B prime pAb
- Gene:
- COPB2 NIH gene
- Name:
- coatomer protein complex subunit beta 2
- Previous symbol:
- -
- Synonyms:
- beta'-COP, betaprime-COP
- Chromosome:
- 3q23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-23
- Date modifiied:
- 2016-04-06
Related products to: Hsp70B prime pAb
Related articles to: Hsp70B prime pAb
- Decreased hepatic removal of low density lipoproteins (LDL) and increased apolipoprotein B (apoB) production cause hypercholesterolemia, a major causal risk factor of atherosclerotic cardiovascular disease (ASCVD). By a genome-wide siRNA screen, we previously identified subunits of the Coat protein I (COPI) complex to limit LDL uptake into Huh-7 hepatocarcinoma cells. - Source: PubMed
Publication date: 2026/06/03
Panteloglou GrigoriosRobert JérômeSmit MariekeHuijkman NicoletteKloosterhuis NielsLaw Christopher SWoods BrianOthman AlaaKleber Marcus EDelgado Graciela ETarugi PatriziaLone Museer AWolters Justina ClarindaRimbert AntoineKerksiek AnjaLütjohann DieterRohrer LuciaZanoni PaoloKakava SofiaHäusler StephanieSchlumpf EvelineFutema MartaHumphries Steve EChou JanetMärz WinfriedGeha Raif SShum Anthony KKuivenhoven Jan Albertvan de Sluis Bartvon Eckardstein Arnold - Immunometabolic remodeling is central to sepsis, yet robust glycolysis-associated biomarkers and their cell-type context remain unclear. - Source: PubMed
Publication date: 2026/05/14
Li TaoLiu YunWang WanZhaoLi QiuYueChen Bing - The coatomer complex has been implicated in cancer progression; however, a comprehensive pan-cancer analysis is lacking. Therefore, it is essential to identify the critical roles and essentiality of coatomer genes across pan-cancer. We systematically profiled the genetic alterations, expression patterns, prognostic relevance, and functional dependencies of all coatomer subunits across multiple cancers using more than 10,000 tumor samples from The Cancer Genome Atlas, complemented by functional perturbation data from CRISPR (n = 1178) and RNAi (n = 707) screens in DepMap. Functional validation was also performed to identify the essentiality of selectively essential coatomer genes in hepatocellular carcinoma (HCC). Gene amplification, most notably of , was the most frequent alteration and was associated with poor survival in bladder and esophageal cancers. Mutations in and also demonstrated prognostic significance in endometrial carcinoma. Expression analyses revealed broad upregulation of coatomer genes across cancer types, with and emerging as strong risk-associated genes (HR > 2). Integrative functional dependency analyses identified as selectively essential in multiple cancers, and its loss was associated with increased drug sensitivity. Functional validation in hepatocellular carcinoma revealed that knockdown impaired malignant phenotypes and reduced tumorigenicity in vivo. Mechanistically, depletion induced Golgi disruption and ER stress, increased ROS production, and suppressed PI3K-AKT signaling, thereby sensitizing cells to sorafenib and doxorubicin. Collectively, this pan-cancer analysis reveals the context-dependent roles of coatomer subunits and identifies as a novel oncogenic driver and potential therapeutic target in HCC, mediating chemoresistance through redox modulation and PI3K-AKT pathway inhibition. - Source: PubMed
Publication date: 2026/02/10
Sen SusmitaDuong Van-ThanhHwang YounginKim SeungmiLee EuijinHan Myoung-EunLee DongjunYoon SikOh Sae-Ock - This study investigated the role of COPB2 in gastric cancer (GC) pathogenesis. Analysis of TCGA datasets and tissue microarrays revealed its upregulation in GC tissues compared to normal adjacent tissues, which was correlated with advanced tumor stage and lymphatic invasion and demonstrated significant diagnostic value (AUC = 0.895 and 0.851). Functional assays using lentiviral-mediated silencing in GC cells showed that COPB2 knockdown suppressed cell proliferation and migration, induced G0/G1-phase arrest, and promoted apoptosis. Mechanistic investigations through microarray, KEGG, and IPA analyses indicated that COPB2 dysregulation inactivated the PI3K/AKT and NF-κB signaling pathways. This led to the downregulation of key oncogenic effectors including Slug, FN1, CDH2, F2RL1, CDK6, CCND1, MMP9, CDKN2A, and SQSTM1, while upregulating tumor suppressors CDKN1B, CDKN1A, and DDIT3. In conclusion, COPB2 acts as an oncogene in GC, driving tumor progression through modulation of the cell cycle and key signaling pathways, highlighting its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/01/31
Li HailongWei DongGao XiaqingSu RongYang ChuntingTang PingYu XiqiuWu Yuhong - Polygenic scores (PGS) predict complex traits and stratify disease risk but often fail to fully capture individual-level variation. "Misaligned" individuals, whose observed phenotypes deviate from their genetically expected values based on polygenic scores (PGS), provide a powerful model for identifying factors beyond common-variant effects, including additional genetic factors. Here, we apply misalignment classification and enrichment testing frameworks to seven continuous and three dichotomous traits, assessing whether misaligned individuals in the UK Biobank are enriched for rare (minor allele frequency (MAF) < 0.1%) damaging genetic variation. We identify significant enrichment (false discovery rate (FDR)-adjusted < 0.05) of predicted loss-of-function (pLoF) variants in and among individuals misaligned for lower-than-expected bone mineral density. We refine previously observed grouped-gene enrichment in individuals with misaligned stature to the single-gene level: shorter-than-expected individuals are enriched for pLoF variants in and , and taller-than-expected individuals are enriched for predicted damaging missense in . Using an individual's misalignment classification as a phenotype, we perform an exome-wide scan across seven traits, resulting in 74 FDR-significant genes. We identify as a gene associated with later age at menopause, potentially protective against primary ovarian insufficiency. For dichotomous disease status traits, we demonstrate evidence for the liability threshold model in the context of counteracting conditionally-orthogonal common and rare variant pathogenic/protective effects. Among individuals diagnosed with type 2 diabetes, carriers of rare pathogenic pLoF variants in and had significantly lower polygenic risk than non-carriers (FDR-adjusted one-sided -test < 5 × 10). We also show that coronary artery disease controls carrying rare protective pLoF variants in had nominally higher polygenic risk (one-sided -test = 0.03) than non-carriers. This study highlights the power of misalignment-based analyses in complex continuous phenotypes and disease, with the potential to validate known genetic contributors to traits and identify novel genes. This work paves the way for better molecular diagnoses and targeted therapeutic discovery. - Source: PubMed
Publication date: 2025/12/31
Baya Nikolas ALassen Frederik HHill BarneyVenkatesh Samvida SCurrant HannahLindgren Cecilia MPalmer Duncan S