PIK3CG Antibody
- Known as:
- PIK3CG Antibody
- Catalog number:
- abx000651
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- PIK3CG Antibody
Related genes to: PIK3CG Antibody
- Gene:
- PIK3CG NIH gene
- Name:
- phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-15
- Date modifiied:
- 2016-10-05
Related products to: PIK3CG Antibody
Related articles to: PIK3CG Antibody
- Glioblastoma (GBM) is one of the most aggressive brain tumors with a poor prognosis despite current treatment modalities. This study aimed to identify genes whose high expression is paradoxically associated with both poor survival and enhanced immune activity, as potential targets for combination chemotherapeutic and immunotherapeutic strategies. - Source: PubMed
Publication date: 2026/04/27
Han Myung-HoonNoh Yung-KyunKim HyunkeeKim Kyu ShikKim Dong-HoonJung Un SukLee Kyung SukKwon Mi JungChae Seoung WanMin Kyueng-Whan - Lung cancer remains a leading cause of cancer mortality in India, yet its genomic landscape remains understudied. To address this gap, we performed whole-exome sequencing (WES) on tumor and matched blood samples from 47 lung cancer patients [adenocarcinoma (ADC): 30; squamous cell carcinoma (SqCC): 10; and small cell lung cancer (SCLC): 7] to comprehensively analyze somatic mutations across all protein-coding genes. Our analysis revealed novel and recurrent alterations, with being the most recurrently mutated gene, and emerging as the most frequently mutated across subtypes. Shared mutations included and , the latter not previously associated with lung cancer. ADC exhibited the highest mutational diversity, particularly in RTK/MAPK pathway genes (). Notably, mutations were identified in 26.7% of ADC cases, including exon 19 deletions (5 cases), exon 21 missense mutations (2 cases), and exon 20 insertions (3 cases) and a novel exon 20 duplication (p.Ser768_Asp770dup). SqCC showed frequent mutations in and , suggesting a role for epigenetic dysregulation. One SqCC case harbored a rare p.Glu866Gly mutation. SCLC was enriched for (43%) and (14%) mutations, along with alterations in and Importantly, therapeutically actionable mutations were identified in 91.5% patients, including those with NCCN-recommended (25.5%) and FDA-approved off-label drug targets (68.1%). These findings underscore the value of WES in uncovering clinically relevant mutations and support the integration of genomic profiling into precision oncology strategies for Indian lung cancer patients. - Source: PubMed
Publication date: 2025/06/06
D'Souza WendyLokesh K NMahajan NareshMishra RadhaAmirtham UshaRajeev L KKumar Arun - Although the molecular mechanism by which wortmannin exerts its anticancer properties in solid tumors is not fully understood, particularly in the context of oral cancer where research is scarce, this study seeks to explore how wortmannin disrupts the PI3K pathway, consequently affecting the proliferation and apoptosis of human oral cancer cells. - Source: PubMed
Kumbhar GauriSuryawanshi PoonamLadke Vaibhav - Comprehensive molecular and phenotypic characterization of tumor models is still needed for a robust understanding of breast cancer mechanisms and therapies. Here, we explore the genome, transcriptome, and proteome of treated and untreated 4T1 triple-negative breast cancer cells to integrate genomic vulnerabilities and mutational profiling with novel treatment-induced delivery, signaling, and apoptotic responses. Nanoencapsulation (AuNPs) of berry-derived polyphenolic compounds was influenced by limited clinical use due to poor stability and bioavailability. Several physicochemical characterizations employed include TEM, FTIR, and targeted UPLC/MS-QQQ assays. We identified significant mutations to breast cancer-related tumor suppressor genes (TP53, BRCA2, BARD1, CDH1, NF1, and CHEK2) and deciphered the functional consequences leveraging the higher throughput Illumina NovaSeq X and NextSeq sequencing and the highly accurate predictive power of AlphaFold. We found ~5,700,000 single-nucleotide variations (SNVs) and 329448 indels, achieving an important upgrade over existing literature data. Multiple sequence alignment with WT mouse and human protein sequences demonstrated that mutations present in 4T1 cells are within highly conserved motifs of key tumor suppressors, emphasizing their relevance to human breast cancer biology. Key findings from differentially expressed gene enrichment analyses (GSEA) revealed positive gene enrichments of DNA repair regulators and TGF-β signaling, while having negative enrichments of cell adhesion, cadherin and MAPK signaling via PI3K/AKT/MAPK/Wnt pathways, potentially influencing apoptosis and immune evasion intrinsic to cancer. Notably, decreased expression of PIK3CG, PALLD, PTPRZ1, and CDH8 and increased expression of SEMA6C, WWOX, NHEJ1, and MAML3 suggested suppression of epithelial-to-mesenchymal transition (EMT) and metastatic potential. Further assessment of immunohistochemical, immunofluorescent, and flow cytometric data revealed that berry-derived nanoparticles are associated with the modulation of oncogenic transcription factors and linked to induced caspase-dependent execution-phase ROS-mediated apoptosis through pPAK1 dephosphorylation, downregulation of pPI3K/pAKT1/mTOR signaling, and modulation of pJAK3/STAT3 pathway supporting transcriptomic and transcriptional reprogramming of 4T1 treated cells. Together, our findings uncover a new strategy to capture berry-derived polyphenols required to regulate apoptosis, autophagy, immune response, and metastasis-related gene networks in breast cancer, thereby underscoring the therapeutic potential of functionalized AuNPs as delivery platforms for dietary phytochemicals. - Source: PubMed
Publication date: 2026/04/10
Fagbohun Oladapo FOladipo Adewale OGao ChengyuOlawoye BabatundeBerry Rachel SCaptain Jaylah CIragena OliveMcDougle XavierHarris Randy JRollins AmandaJoseph Jitcy SFadare Olatomide AKincaid Russell - Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes a cAMP-activated chloride channel, cause cystic fibrosis (CF), the most common life-threatening inherited disorder among White individuals. Current CFTR correctors and potentiators, such as elexacaftor-tezacaftor-ivacaftor (ETI), only partially restore the function of the most prevalent mutant, F508del-CFTR, resulting in residual disease in people with CF. Here, we demonstrate that a mimetic peptide targeting the A-kinase-anchoring protein (AKAP) function of PI3Kγ (PI3Kγ MP), and driving localized cAMP elevation, enhances F508del-CFTR membrane localization, maximizing ETI efficacy in restoring chloride secretion. Mechanistically, PI3Kγ MP activates an AKAP-Lbc-anchored pool of PKD1, a known regulator of membrane trafficking. Consistently, PKD1 inhibition prevents PI3Kγ MP from enhancing the membrane expression of ETI-corrected F508del-CFTR. Overall, our findings reveal a regulatory pathway controlling CFTR membrane abundance via the AKAP function of PI3Kγ, which can be targeted to overcome the limitations of current CFTR modulator therapies. - Source: PubMed
Publication date: 2026/03/23
Murabito AlessandraMergiotti MarcoCapurro ValeriaLoffreda AlessiaLi MingchuanPeretto PaolaRen KaiRaimondi AndreaTacchetti CarloDiviani DarioPedemonte NicolettaHirsch EmilioGhigo Alessandra