RACGAP1 pSer387 antibody Ab
- Known as:
- RACGAP1 pSer387 (anti-) Antibody
- Catalog number:
- 1487979
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- RACGAP1 pSer387 antibody
Related genes to: RACGAP1 pSer387 antibody Ab
- Gene:
- RACGAP1 NIH gene
- Name:
- Rac GTPase activating protein 1
- Previous symbol:
- -
- Synonyms:
- MgcRacGAP
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-09
- Date modifiied:
- 2015-08-25
Related products to: RACGAP1 pSer387 antibody Ab
Related articles to: RACGAP1 pSer387 antibody Ab
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Sharma Manish KChongtham JonitaBhushan AshishChosdol KunzangSinha SubrataSrivastava Tapasya - Cervical cancer continues to pose a considerable challenge to global health, necessitating innovative approaches for improved diagnostics and personalized treatment strategies. Prior investigations have suggested that plasma proteins may play a role in the pathogenesis of cervical cancer; however, these studies do not confirm a causal relationship. To address this gap, conducted a large-scale Mendelian randomization (MR) study of the plasma proteome. - Source: PubMed
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Zhao Yan-HongRuan Qing-FenNing Jing-HuaZhang XinQu RunZou JingLiang YiZhang Cheng-GuiZhang Yu-Zhe - A central objective in oncology is to identify therapeutic targets essential for the survival of proliferating malignant cells. However, a major challenge in pre-clinical research is the scarcity of robust models capable of accurately assessing therapeutic efficacy in patient-specific heterogeneous cancer cells. Here, we developed an ex vivo platform for patient-specific assessment using biomacromolecule-based targeting delivery systems for CRISPR-Cas9 mediated gene knockout and in situ mRNA profiling in patient-derived circulating malignant cells (CMCs). Using a cancer targeting vector, we conducted a personalized evaluation of the impact of Rac GTPase activating protein 1 (RACGAP1) knockout on cell growth in a cancer cell line and patient-derived heterogeneous CMCs. RACGAP1 knockout induced irreversible cytokinesis failure, leading to markedly reduced proliferation and invasion capacity, DNA damage, and increased apoptosis. Our approach establishes a promising strategy for the personalized validation of novel therapeutic targets. - Source: PubMed
Publication date: 2026/06/27
Gao Qing-YuHan DiLiao Xin-RuLei Jin-JuQi Li-JinHuang Qi-YangFu Fei-FeiCheng Si-Xue - Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality worldwide; molecular biomarkers that reflect hepatitis B virus (HBV)/hepatitis C virus (HCV)-associated tumor biology and predict prognosis or therapeutic vulnerabilities are needed. The research is a secondary analysis of public data (secondary data analysis) based on Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) data to identify differentially expressed genes (DEGs) common to HBV-HCC, HCV-HCC, and non-viral HCC datasets. Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, protein-protein interaction (PPI) network analysis, and hub-gene selection were then performed. Differential expression, prognostic association, immune-infiltration, and drug-sensitivity correlations were also analyzed. Eighty common DEGs (73 upregulated, 7 downregulated) were identified. PPI topological analysis yielded 53 hub genes; five genes and , were prioritized and validated as significantly upregulated in liver HCC and associated with poorer overall survival. Immune deconvolution showed consistent positive correlations between the hub genes and B cells and regulatory T cell subsets, and negative correlations with mucosal-associated invariant T (MAIT) cells, macrophages, and natural killer (NK)/monocyte signatures. Drug-gene correlation analysis revealed positive associations of and with sensitivity to mitogen-activated protein kinase inhibitors and negative correlations with several targeted inhibitors. The identified prognostically unfavorable hub genes in HBV/HCV-associated HCC are associated with an immunosuppressive microenvironment and with patterns of drug sensitivity. - Source: PubMed
Publication date: 2026/04/27
Safarnezhad Tameshkel FahimehSadat Kalaki NiloufarKarimi ElhamRazizadeh Mohammad HosseinHaidar Abed El HasanAmiri AliZaki MohammadrezaNikkhah MehdiKarbalaie Niya Mohammad Hadi - Investigation of in utero, tissue-specific molecular pathways contributing to prenatal programming of childhood-onset asthma is needed to develop effective, targeted prevention strategies. We aimed to examine the relationship between predicted gene expression in placenta and childhood-onset asthma and to compare relationships between childhood- and adult-onset asthma. Asthma genome-wide association study published summary statistics were obtained from the UK Biobank and published placental gene expression quantitative trait loci were obtained from the Rhode Island Child Health Study. We used S-PrediXcan to evaluate and compare associations between placental predicted gene expression and childhood- and adult-onset asthma and to determine whether signals were placenta-specific. Among 8,038 tested placental predicted expression-asthma associations, we identified 56 (0.7%) genes only significantly associated with childhood-onset asthma, 12 (0.1%) genes only significantly associated with adult-onset asthma, and 18 (0.2%) shared genes. Predicted expression of several genes (ACTL9, AMN, C9orf38, C11orf30, CTSE, EFCAB13, EIF4E1B, FN1, GLS2, IL6, IVL, LZIC, MAN2A2, MEGT1, RACGAP1, SMAD6, SPATA5, TMEM25, VTI1B, WDR19) was not significantly associated with childhood- or adult-onset asthma in any non-placental tissue, suggesting that the associations may be placenta-specific. This study identified alterations in predicted expression of placental genes associated with transcriptional pathways critical to the development of asthma. We identified unique and shared pathways, particularly related to immune regulation, associated with childhood- and adult-onset. This expands our understanding of the fetal origins of asthma, highlights the placenta as an informative tissue in understanding asthma pathogenesis, and identifies target genes to prioritize for future functional studies. - Source: PubMed
Publication date: 2026/05/13
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