BCAR1 ELISA kit
- Known as:
- BCAR1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-BCAR1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- BCAR1 ELISA kit
Related genes to: BCAR1 ELISA kit
- Gene:
- BCAR1 NIH gene
- Name:
- BCAR1 scaffold protein, Cas family member
- Previous symbol:
- -
- Synonyms:
- P130Cas, Crkas, CAS, CASS1
- Chromosome:
- 16q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-29
- Date modifiied:
- 2019-01-25
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- Sudden cardiac death (SCD) is a leading cause of global mortality, with coronary artery disease (CAD) being the primary etiology. Vascular smooth muscle cell (VSMC) migration and proliferation, regulated by actin cytoskeletal dynamics, are pivotal to CAD pathogenesis. The integrin-focal adhesion-cytoskeleton signaling axis modulates these processes; however, its genetic contribution to SCD-CAD remains poorly understood. In this case-control study of a southern Chinese Han population (239 SCD-CAD cases; 594 healthy controls), we investigated 10 insertion-deletion (indel) polymorphisms across eight key genes within this axis. Using multiplex fluorescent PCR and capillary electrophoresis (CE), followed by logistic regression and haplotype analyses, we identified three protective variants: rs10599004 (OR = 0.78, p = 0.018), rs143263543 (OR = 0.70, p = 0.024), and rs58213835 (OR = 0.80, p = 0.046). Additionally, a significant risk haplotype was identified in BCAR1 (ins-rs149617239-ins-rs58213835, p = 0.007). Mendelian randomization (MR) analysis further supported the causal roles of genetically predicted BCAR1, CRK, and DOCK1 expression in cardiovascular risk. These findings underscore the involvement of this signaling axis in SCD-CAD susceptibility and suggest these genetic markers as potential tools for cardiovascular risk assessment as well as forensic molecular autopsy. Further validation through large-scale cohort studies and functional assays is essential to fully elucidate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/05/08
Cai MengqiHe YanMeng HaoliangLuo BinGao Yuzhen - Chemotherapy resistance remains a critical bottleneck limiting its clinical efficacy in small cell lung cancer (SCLC), with its core mechanisms and targeted intervention strategies urgently requiring breakthroughs. Our study revealed that the BMX (bone marrow tyrosine kinase on chromosome X)-E2F1 (E2F transcription factor 1) axis is a pivotal regulator of chemoresistance in SCLC. Synchronous upregulation of phosphorylated BMX (Tyr566) and E2F1 was observed in SCLC tissues and cells. Mechanistically, BMX stabilized E2F1 via the ERK1/2 (extracellular signal-regulated kinase 1/2)-Cyclin D1/CDK4/6 (cyclin-dependent kinase 4/6) signaling axis, phosphorylating E2F1 at Ser332/337 and inhibiting its degradation via the ubiquitin-proteasome pathway. Inhibition or knockdown of BMX reduced E2F1 stability, promoting its degradation and reversing chemoresistance. E2F1 knockdown decreased the expression of genes associated with cell cycle regulation, migration, invasion, and DNA repair, further sensitizing chemoresistant SCLC cells to cisplatin. We also discovered IHMT-15137, a potent and selective BMX inhibitor. In vitro studies using SCLC patient-derived cells (PDCs)/patient-derived organoids (PDOs) and chemoresistant cell lines revealed that IHMT-15137, combined with cisplatin, synergistically induced cell cycle arrest, apoptosis, and DNA damage while suppressing cell migration and invasion. In vivo xenograft models demonstrated that the combination significantly inhibited tumor growth without causing significant toxicity. Our findings reveal the molecular mechanisms of SCLC chemoresistance and suggest potential therapeutic strategies targeting the BMX-E2F1 axis to overcome this challenge. - Source: PubMed
Publication date: 2026/04/08
Wu TingQi ShuangShi ChenliangWu ChaoLiu QingwangHu ChenHu JieWang AoliLiu JingQi ZipingWang WenchaoLiu Qingsong - Genome-wide association studies (GWAS) have identified thousands of non-coding variants associated with complex traits and diseases. However, it remains challenging to pinpoint the causal genes that are regulated by associated genetic variants. Connecting causal non-coding variants with genes can rely on methods that identify direct physical interactions (e.g. chromosome conformation capture) or on probabilistic models that predict regulatory links. These statistical models take advantage of gene expression and chromatin accessibility profiles generated in cells and tissues by bulk or single-cell (sc) methodologies. Here, we tested whether using bulk or sc RNAseq/ATACseq data and corresponding predictive enhancer-to-gene models impact the prioritization of causal GWAS genes. Using non-treated and TNFα-treated human endothelial cells as a well-controlled experimental system, we show that bulk and sc RNAseq/ATACseq profiles are similar and highlight the same biology (e.g. biological pathways). Despite these similarities, we show using GWAS results for coronary artery disease (CAD) and diastolic blood pressure that applying enhancer-to-gene models designed for bulk or sc methodologies can yield differences in terms of captured heritability, fine-mapped variants and linked genes. For instance, at one CAD locus, the bulk-based ABC model predicts a regulatory link with , whereas the sc-based model scE2G prioritizes a different gene ( ). On the same experimental model, our results indicate that choosing between a bulk or sc approach will influence regulatory link model predictions; this should be considered when planning functional experiments to characterize GWAS discoveries. - Source: PubMed
Publication date: 2026/05/27
Zevounou JenniferLo Ken SinMcGinnis Christopher SSatpathy Ansuman TLettre Guillaume - Around 30% of patients with hormone receptor-positive (HR+) breast cancer acquire resistance to endocrine therapy combined with cyclin-dependent kinase 4/6 inhibitors (CDK4/6i), which are first-line treatments in metastatic settings. Therefore, we aimed to identify loci associated with resistance to endocrine therapy and CDK4/6i; this was achieved using retroviral vectors, which randomly insert gene-disrupting elements into the genome, causing gene expression alterations and potentially leading to therapy resistance. ER-positive ZR75.1 breast cancer cells transduced with retroviral vectors were treated with endocrine (tamoxifen, fulvestrant) or CDK4/6i monotherapies (abemaciclib, palbociclib, ribociclib) or a combination of fulvestrant and ribociclib. DNA was extracted, and virus integration sites (VISs) were characterized according to the detection frequency and read depth using next-generation sequencing (VIS-NGS). Resistance-associated VIS loci were identified when differentially presented in treated samples compared to controls. Well-established tamoxifen resistance genes (, , ) were detected, enabling the validation of our approach. Thirty-seven VIS loci were associated with resistance to fulvestrant and ribociclib monotherapies. Twenty of these loci were also identified as candidates for resistance to other CDK4/6i and to fulvestrant and ribociclib combination therapy, including and -genes that are involved in resistance to endocrine therapy but have not yet been associated with resistance to CDK4/6i. The identification of unique and shared resistance-associated loci highlights the complexity of resistance pathways. - Source: PubMed
Publication date: 2026/01/29
Huang ZhangzanBeaufort CorineHelmijr JeanZantboer BrianRozema GiadaMuritti CamillaWhien Julia JUijterwegen AnnaMassimino MicheleMartens John W MJansen Maurice P H M - Several vascular diseases including coronary artery disease, hypertension, stroke, and abdominal aortic aneurysm, have significant genetic underpinnings. Genome-wide association studies have unveiled many genetic loci associated with one or more of these diseases. However, the causative genes at most of these loci are yet to be determined, which hampers the translation of the genetic findings into a better understanding of the disease mechanisms and the identification of new therapeutic targets. Here, in an integrative functional genomics analysis of these loci, we identify a panel of likely causal genes, some of which are pleiotropic for more than one of these vascular diseases. Pooled CRISPR knockout screen analyses of these likely causal genes indicate that many of them influence vascular smooth muscle cell behaviour, and validation experiments of selected genes confirm that FES, BCAR1, CARF and SMARCA4 exert such effects. Further functional experiments focusing on FES, a pleiotropic gene for both coronary artery disease and hypertension, show that it modulates the expression of genes involved in vascular remodeling and that Fes knockout in mice promotes atherosclerosis as well as raises blood pressure. These findings provide an insight into the genetic basis of vascular diseases and inform targets for therapeutic development. - Source: PubMed
Publication date: 2026/02/05
Solomon Charles UMcVey David GAndreadi CatherineGong PengTurner LenkaSong Dedrick S SZhang HemingLee Dominic PKaramanavi ElisavetYang WeiChu JiapengChen RunjiHaworth Kim EAnene-Nzelu Chukwuemeka GeorgeLi HuiDenniff Matthew JLi Peter YZhang YanhongHuang XiaoxinMorris Gavin EGreer Peter AStringer Emma JYu HaojieFoo Roger S YDouglas GillianSamani Nilesh JWebb Tom RYe Shu