PIK3C2A
- Known as:
- PIK3C2A
- Catalog number:
- Y213331
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PIK3C2A
Related genes to: PIK3C2A
- Gene:
- PIK3C2A NIH gene
- Name:
- phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha
- Previous symbol:
- -
- Synonyms:
- PI3K-C2alpha
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-21
- Date modifiied:
- 2016-10-05
Related products to: PIK3C2A
anti-PIK3C2Aanti-PIK3C2Aanti-PIK3C2A (3E7)anti-PIK3C2A (3E7)anti-PIK3C2A (3E7)anti-PIK3C2A (3E7) type: Primary antibodies host: MouseAnti-PIK3C2A (3E7), Mouse Monoclonal to PIK3C2A, Isotype IgG1, Host Mouseanti-PIK3C2A type: Primary antibodies host: MouseAntibodies: PIK3C2A HOST: Goat Clonality: pAbCpk,Cpk-m,Mouse,Mus musculus,p170,Phosphatidylinositol-4-phosphate 3-kinase C2 domain-containing subunit alpha,Phosphoinositide 3-kinase-C2-alpha,PI3K-C2-alpha,Pik3c2a,PtdIns-3-kinase C2 subunit alphaELISA Kit FOR Phosphatidylinositol-4-phosphate 3-kinase C2 domain-containing subunit alpha; organism: Mouse; gene name: Pik3c2aELISA Kit for Phosphoinositide 3-Kinase Class 2 Alpha Polypeptide (PIK3C2a)ELISA Kit for Phosphoinositide 3-Kinase Class 2 Alpha Polypeptide (PIK3C2a)ELISA Kit for Phosphoinositide 3_Kinase Class 2 Alpha Polypeptide (PIK3C2a) Organism Homo sapiens (Human)ELISA Kit for Phosphoinositide 3_Kinase Class 2 Alpha Polypeptide (PIK3C2a) Organism Mus musculus (Mouse) Related articles to: PIK3C2A
- Integration of Epstein-Barr virus (EBV) DNA into the human genome is a critical event in nasopharyngeal carcinogenesis. Here, we comprehensively characterize large-scale virus-human integration events in three EBV-positive nasopharyngeal carcinoma (NPC) cell lines and one patient NPC tumor using Nanopore long-read sequencing technology. We identified four distinct integration types, with Type A being particularly prevalent, characterized by the integration of a single fragment of the EBV genome followed by human DNA. Our findings reveal the involvement of multiple integration events in inducing inter-chromosomal translocations, leading to significant genomic disruption through chromosomal rearrangements. Additionally, we explore the relationship between EBV integration sites and structural variations, further supporting the role of EBV integration in driving genomic instability. By integrating RNA-seq data, we demonstrate the potential for EBV integration to disrupt gene expression, highlighting several integration sites within cancer-associated genes such as CD96, ARHGAP27, ASH1L, KDM3B, ZMYM2, and PIK3C2A. Notably, EBV-human fusion events were prevalent in EBV-associated NPCs, including intriguing fusion transcripts such as LRRC8C-RPMS1 and LINC00486-RPMS1, which provide further evidence of the oncogenic potential of EBV integration. Taken together, this study uncovers EBV integration patterns in Nasopharyngeal carcinogenesis using long-read sequencing technology. - Source: PubMed
Publication date: 2026/05/12
Kardan ZahraKadam AdwayChai Annie Wai YeengCheong Sok ChingLoganathan Sampath Kumar - Intervertebral disc degeneration (IDD) is a prevalent disease with an increasing incidence, and aging is a key risk factor for its progression. Therefore, this study aimed to explore the role of aging-related genes in IDD through bioinformatics analysis. Differentially expressed aging-related genes were obtained from the CellAge, GSE150408 and GSE124272 datasets, followed by biomarker screening via machine learning. Finally, the identified biomarkers were validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western Blot (WB), and immunohistochemistry (IHC) assays. A total of 33 aging-related differentially expressed genes (DEGs) were screened in IDD, and machine learning combined with ROC curve analysis identified PPM1D, PIK3C2A, and BTG3 as aging-related biomarkers for IDD; Gene Set Enrichment Analysis (GSEA) revealed that these three biomarkers were enriched in gene functions including cellular senescence, multicellular organismal aging, negative regulation of cellular senescence, and Ribosome. In addition, the multifactorial regulatory network showed that transcription factor E2F1 and hsa-miR-147 co-regulated both PPM1D and BTG3. In experiments validating biomarker expression levels, BTG3 and PIK3C2A exhibited consistent expression trends across IHC, RT-qPCR, WB assays and the two datasets. BTG3 and PIK3C2A may play more critical roles in the progression of IDD, thereby providing novel insights for the development of new therapeutic strategies for IDD patients. - Source: PubMed
Publication date: 2026/04/09
Zhang FanYuan LeiDing HengLou ZhenkaiLi Xingguo - As society ages, the prevalence of spinal degenerative diseases (SDDs) is rising, creating significant life and financial burdens for patients and their families. This study employs mendelian randomization (MR) to identify therapeutic targets for SDDs management. Two sample mendelian randomization (TSMR) analyses were conducted to investigate the causal relationships between multiple genes and various SDDs, including osteoporosis (OP), spinal canal stenosis (SCS), and prolapsed disc/slipped disc (PD/SD). To enhance the robustness of the findings, summary data-based MR (SMR) analyses were performed, complemented by Bayesian co-localization, which provided strong evidential support for the results. Additionally, the potential therapeutic applications were assessed through estimates of druggability. Our findings reveal several target genes linked to the risk of SDDs. Notably, ESR1 was positively and causally associated with the risk of osteoporosis (OR: 1.011, 95% CI: 1.008-1.016, P = 2.41 × 10). Conversely, high expression of HTT was associated with a reduced risk of spinal canal stenosis (OR: 0.693, 95% CI: 0.589-0.816, P = 1.06 × 10). Furthermore, high expression of PIK3C2A was linked to increased risk of spinal canal stenosis (OR: 1.086, 95% CI: 1.056-1.117, P = 9.01 × 10). In conclusion, this study identifies several potential therapeutic targets related to SDDs and offers new insights for the development of therapeutic agents aimed at managing these conditions. - Source: PubMed
Publication date: 2026/04/02
Qin HaoHao MingyuWang ZhitanZhang JingXie MinghaoDiao YuhangHu XiaojunRong HongtaoZhu Tao - Oculoskeletodental syndrome (OCSKD) is a rare ciliopathy characterized by dysmorphic facial features, congenital cataracts, dental and skeletal anomalies, developmental delays, and strokes. PIK3C2A plays a crucial role in membrane trafficking and various intracellular signaling pathways by synthesizing lipid messengers. To date, only two studies describing four families have linked PIK3C2A loss-of-function variants to OCSKD, with limited functional analyses in primary cell lines. - Source: PubMed
Publication date: 2026/03/02
Al-Rashdi MaryamAl-Hadabi AbirMameesh MahaGanesh AnuradhaAl-Maawali AlmundherAl-Azri Fakhriya - Oculoskeletodental syndrome (OCSKD) is a rare autosomal recessive ciliopathy caused by PIK3C2A loss-of-function variants, characterized by ocular, skeletal, and dental anomalies. Ocular findings most commonly include cataract and secondary glaucoma; however, high axial myopia and megalocornea have not been previously reported in the literature. - Source: PubMed
Publication date: 2026/02/17
Pawar NeelamR MeenakshiJ AnupamaA FathimaLakshmi SaiKk Shafna