Human Polyclonal PIK3CA Ab
- Known as:
- Human Polyclonal PIK3CA Antibody
- Catalog number:
- a0265
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal PIK3CA
Related genes to: Human Polyclonal PIK3CA Ab
- Gene:
- PIK3CA NIH gene
- Name:
- phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha
- Previous symbol:
- -
- Synonyms:
- PI3K
- Chromosome:
- 3q26.32
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-15
- Date modifiied:
- 2019-04-23
Related products to: Human Polyclonal PIK3CA Ab
Related articles to: Human Polyclonal PIK3CA Ab
- - Source: PubMed
Publication date: 2026/06/30
Zhang HongyanZhang LonglongHe YunaJiang DeweiSun JianLuo QianmeiLiang HuichunWang TiantianLi FubingTang YuYang ZimoLiu WenjingRao YuChen Ceshi - Grass carp (Ctenopharyngodon idella) is a major aquaculture species, yet production efficiency is often constrained by growth performance and metabolic disorders such as hepatic lipid deposition. Conventional selective breeding faces challenges in further improving these complex traits, necessitating precision genetic interventions. In this study, we combined comparative transcriptomics with CRISPR/Cas9 mediated gene disruption to investigate the regulatory role of Pik3r1. Comparative RNA-seq of fast- and slow-growing individuals together with protein-protein interaction network analysis identified Pik3r1 as a candidate negative regulator of growth. To validate its function, we generated Pik3r1 mosaic F0 mutants by targeting the SH3 domain of Pik3r1. Disruption of Pik3r1 conferred a profound growth advantage, increasing body weight by 51.8% and body length by 13.5% compared to wild-type controls. Histological analyses revealed that enhanced muscle accretion was driven by both hypertrophy with a 22.50% increase in myofiber cross-sectional area and hyperplasia characterized by an 18.90% rise in fiber density, coupled with a 67.7% reduction in hepatic lipid accumulation. At the molecular level, Pik3r1 disruption relieved the inhibitory effect on the PI3K/AKT/mTOR cascade, with upregulation of PI3K, AKT, mTOR, S6K1, Myod1, and Mybpc1 and downregulation of 4ebp1 and Pik3ca in muscle, accompanied by upregulation of PPARα and CPT1a and downregulation of FASN and ACC1 in the liver. Furthermore, a clear genotype phenotype correlation was observed: fish carrying confirmed premature termination codons exhibited substantially greater growth enhancement (77.6% increase in body weight) than those with in-frame mutations. Collectively, our results support Pik3r1 as a key regulator linking somatic growth and lipid metabolism in grass carp, and highlight its potential as a target for molecular breeding aimed at improving yield and carcass quality. - Source: PubMed
Publication date: 2026/06/30
Lv WenyaoMeng XinzhanSun TianyangChen YuxuanLi WeizhongSheng TaoCong QianYu QiaozhenHe RuitaoHe RuicongShen YubangRen JianfengQiu JunqiangGui LangLi JialeXu Xiaoyan - High-risk human papillomavirus (HPV) infection, particularly HPV16, is a major etiological factor associated with multiple human cancers, including anal, cervical and oropharyngeal carcinomas. However, the mechanisms underlying tissue-specific responses to HPV oncogene expression remain poorly understood. Here, we developed and characterized a double-inducible transgenic mouse model enabling spatially and temporally controlled expression of HPV16 E6/E7 oncoproteins in K14-positive epithelial progenitor cells of both the anal and oral mucosa. Within two months of induction, HPV16-E6/E7 expression elicited epithelial hyperplasia and dysplasia in both tissues, but with distinct outcomes: low-grade squamous intraepithelial lesions in the anal canal and moderate to severe dysplasia in the tongue. Continuous oncogene expression was required for lesion maintenance, as doxycycline withdrawal reversed the proliferative phenotype, indicating a dynamic and reversible process. To assess whether activation of the PI3K pathway could cooperate with HPV oncogenes, we combined the E6/E7 model with a Pik3caH1047R knock in mouse line. Constitutive PI3K activation alone induced mild dysplasia in both epithelia, whereas its combination with E6/E7 enhanced dysplastic severity in the tongue but not in the anal mucosa. No progression to invasive carcinoma was observed within six months. These findings demonstrate that identical oncogenic signals-HPV16 E6/E7 expression and PI3K activation-produce distinct premalignant outcomes depending on epithelial context. This work highlights the critical role of local microenvironmental factors in HPV-driven carcinogenesis and provides a platform to identify tissue-specific therapeutic vulnerabilities in HPV-associated cancers. - Source: PubMed
Publication date: 2026/06/30
Ayre MarinaFernandez-Ugazio GonzaloDiGaudio Anabel VCoso Omar AdriánGutkind J SilvioRaimondi Ana Rosa - Pulmonary adenosquamous carcinoma (ASC) is a rare, aggressive subtype of non-small cell lung cancer (NSCLC), characterized by both adenocarcinoma (ACC) and squamous cell carcinoma (SCCC) components. Due to its rarity, the clonal origin, evolutionary drivers, and tumor microenvironment (TME) of ASC remain poorly understood. - Source: PubMed
Publication date: 2026/06/15
Zhang XiuwenWu HengZhao WenhaoHu ZixuanWang GuannanLi YongwenLi XuanguangZhang HongbingLiu MinghuiChen ChenLiu JinghaoZhou WenhaoLiu HongyuChen Jun - Malignant effusions in breast cancer are a minimally invasive source for molecular profiling. Effusion-derived cytology specimens, cell blocks (CB) and post-ThinPrep PreservCyt (PTPC) supernatant, are reliable sources for molecular testing but differ in DNA concentration and turnaround time (TAT). This study evaluates mutational profiles, cytology characteristics, and clinical correlates to assess the utility of effusion-based molecular testing in breast cancer. - Source: PubMed
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