APH1A Antibody
- Known as:
- APH1A Antibody
- Catalog number:
- AF1072a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- APH1A Antibody
Ask about this productRelated genes to: APH1A Antibody
- Gene:
- APH1A NIH gene
- Name:
- aph-1 homolog A, gamma-secretase subunit
- Previous symbol:
- -
- Synonyms:
- APH-1A, CGI-78
- Chromosome:
- 1q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-08
- Date modifiied:
- 2016-05-16
Related products to: APH1A Antibody
Related articles to: APH1A Antibody
- : The Notch signaling pathway regulates cell fate, proliferation, and differentiation, and its dysregulation has been implicated in various cancers, including breast cancer. MicroRNAs (miRNAs) are critical post-transcriptional regulators that can modulate Notch pathway components. The aim of this study was to identify miRNAs that may potentially regulate the expression of Notch pathway-related genes across five molecular subtypes of breast cancer in Polish women. : Tumor and adjacent normal tissue samples were collected from 405 patients with five breast cancer subtypes: luminal A ( = 130), HER2-negative luminal B ( = 100), HER2-positive luminal B ( = 96), non-luminal HER2-positive ( = 36), and triple-negative breast cancer ( = 43). Gene expression was profiled using mRNA microarrays and validated with RT-qPCR and ELISA. Candidate regulatory miRNAs were identified by miRNA microarrays and confirmed using the miRDB database. : , , , , , , , , and were consistently dysregulated across all breast cancer subtypes. Overexpression of and may be driven by decreased levels of miR-145, miR-98, and miR-381. Conversely, downregulation of may be associated with elevated expression of miR-196a and miR-155. No regulatory miRNAs meeting the selection criteria were identified for , , , , , or . : The consistent alterations suggest the presence of a shared Notch-driven oncogenic signature in breast cancer, potentially driving cell proliferation, stemness, and resistance to therapy. These findings enhance our understanding of Notch signaling in breast cancer and propose novel miRNA-Notch interactions as candidate targets for therapeutic intervention. - Source: PubMed
Publication date: 2025/12/12
Mitka-Krysiak ElżbietaKról-Jatręga KatarzynaOssowski PiotrZmarzły NikolaBereza KrzysztofOrdon PawełKulej WojciechSirek TomaszSirek AgataBoroń KacperBoroń MaciejBoroń DariuszGrabarek Beniamin Oskar - Cardiotoxicity, particularly drug-induced arrhythmias, poses a significant challenge in drug development, highlighting the importance of early-stage prediction of human ether-a-go-go-related gene (hERG) toxicity. hERG encodes the pore-forming subunit of the cardiac potassium channel. Traditional methods are both costly and time-intensive, necessitating the development of computational approaches. In this study, we introduce AttenhERG, a novel graph neural network framework designed to predict hERG channel blockers reliably and interpretably. AttenhERG demonstrates improved performance compared to existing methods with an AUROC of 0.835, showcasing its efficacy in accurately predicting hERG activity across diverse datasets. Additionally, uncertainty evaluation analysis reveals the model's reliability, enhancing its utility in drug discovery and safety assessment. Case studies illustrate the practical application of AttenhERG in optimizing compounds for hERG toxicity, highlighting its potential in rational drug design.Scientific contributionAttenhERG is a breakthrough framework that significantly improves the interpretability and accuracy of predicting hERG channel blockers. By integrating uncertainty estimation, AttenhERG demonstrates superior reliability compared to benchmark models. Two case studies, involving APH1A and NMT1 inhibitors, further emphasize AttenhERG's practical application in compound optimization. - Source: PubMed
Publication date: 2024/12/23
Yang TianbiaoDing XiaoyuMcMichael ElizabethPun Frank WAliper AlexRen FengZhavoronkov AlexDing Xiao - The NOTCH-signaling pathway is responsible for intercellular interactions and cell fate commitment. Recently, NOTCH pathway genes were demonstrated to play an important role in aortic valve development, leading to an increased calcified aortic valve disease (CAVD) later in life. Here, we further investigate the association between genetic variants in the NOTCH pathway genes and aortic stenosis in a case-control study of 90 CAVD cases and 4723 controls using target panel sequencing of full-length 20 genes from a NOTCH-related pathway (, , , , , , , , , , , , , , , , , , , ). We identified a common intronic variant in , protecting against CAVD development (rs3812603), as well as several rare and unique new variants in NOTCH-pathway genes (, , , , , , ), with a prominent effect of the protein structure and function. - Source: PubMed
Publication date: 2024/07/17
Irtyuga OlgaSkitchenko RostislavBabakekhyan MaryUsoltsev DmitriiTarnovskaya SvetlanaMalashicheva AnnaFomicheva YulyaRotar OksanaMoiseeva OlgaShadrina UlyanaArtomov MykytaKostareva AnnaShlyakhto Evgeny - The aim of this study is to screen the differentially expressed genes and genes with alternative splicing in PPIA overexpressing cells by transcriptome sequencing. Transcriptome sequencing was performed to identify differentially expressed genes and genes with altered alternative splicing in PPIA overexpressing cells and results were validated by real-time quantitative polymerase chain reaction. The biological function and pathways of those genes were further explored through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses. A total of 157 significantly upregulated genes and 171 significantly downregulated genes were identified in PPIA overexpressing cells, and the splicing pattern of LHPP, APH1A, BRD1, and ORAI3 was found to be altered. GO analyses showed that the most enriched GO terms of the 157 upregulated genes included extracellular region, protein binding, and metal ion, and the most enriched GO terms of the 171 downregulated genes included binding neuron projection, protein binding, and endoplasmic reticulum unfolded protein response. Kyoto Encyclopedia of Genes and Genomes analyses showed that the 157 upregulated genes were mainly enriched in gastric acid secretion, Mitogen-activated protein kinase signaling pathway, etc, and the 171 downregulated genes were mainly enriched in transcriptional misregulation in cancer, Tumor necrosis factor signaling pathway, etc. The overexpression of PPIA in human umbilical vein endothelial cells causes changes in the expression of downstream genes and induces alternative splicing in multiple genes. PPIA alters the expression or the alternative splicing pattern of downstream genes, leading to pathogenesis of vascular endothelial injury by high glucose mediated through CyPA. - Source: PubMed
Yang WenwenZhou XinRongLi QiujuYin MingyueWang Ning - Chronic obstructive pulmonary disease (COPD) is a prevalent condition that significantly impacts public health. Unfortunately, there are few effective treatment options available. Mendelian randomization (MR) has been utilized to repurpose existing drugs and identify new therapeutic targets. The objective of this study is to identify novel therapeutic targets for COPD. - Source: PubMed
Publication date: 2024/04/10
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