PI 3-kinase p85 alpha Antibody (D-3): sc-377482

PI 3-kinase p85α Antibody (D-3) is a mouse monoclonal IgM kappa antibody targeting an epitope mapped between amino acids 27-65 near the N-terminus of human PI 3-kinase p85α, with reactivity in mouse, rat, and human species. Anti-PI 3-kinase p85α antibody (D-3) is validated for applications including western blotting (WB), immunoprecipitation (IP), immunofluorescence (IF), immunohistochemistry with paraffin-embedded sections (IHCP), and enzyme-linked immunosorbent assay (ELISA). PI 3-kinase p85α, also known as PIK3R1 or phosphoinositide 3-kinase regulatory subunit alpha, functions as a critical adapter protein in the phosphatidylinositol 3-kinase (PI3K) complex. PI 3-kinase p85α regulates the activity of the catalytic p110 subunit by anchoring to receptor tyrosine kinases and ensuring proper cellular localization. Post-translational modifications, including tyrosine phosphorylation, play a pivotal role in modulating PI 3-kinase p85α′s function and interactions with other signaling proteins, thereby fine-tuning pathways such as AKT/mTOR signaling that govern cell growth, survival, and metabolism. Additionally, ubiquitination of PI 3-kinase p85α affects stability and turnover, highlighting the importance of these modifications in maintaining signaling fidelity. SH3 and SH2 domains of PI 3-kinase p85α enable interaction with phosphorylated tyrosine residues on activated receptors, a crucial step in initiating PI3K-dependent signaling cascades. Dysregulation of PI 3-kinase p85α due to mutations or altered post-translational modifications is linked to cancer and metabolic disorders. PI 3-kinase p85α monoclonal antibody (D-3) serves as an essential tool for exploring regulatory mechanisms and signaling roles in normal and pathological contexts.

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PI 3-kinase p85 alpha Antibody (D-3) References:

1. Genetic disruption of the PI3K regulatory subunits, p85α, p55α, and p50α, normalizes mutant PTPN11-induced hypersensitivity to GM-CSF.  |  Goodwin, CB., et al. 2012. Haematologica. 97: 1042-7. PMID: 22315502
2. Autosomal dominant PIK3R1 mutations cause SHORT syndrome.  |  Chung, BK. and Gibson, WT. 2014. Clin Genet. 85: 228-9. PMID: 24033310
3. Signal transducer and activator of transcription 3 and the phosphatidylinositol 3-kinase regulatory subunits p55α and p50α regulate autophagy in vivo.  |  Pensa, S., et al. 2014. FEBS J. 281: 4557-67. PMID: 25205393
4. The Opposing Roles of PIK3R1/p85α and PIK3R2/p85β in Cancer.  |  Vallejo-Díaz, J., et al. 2019. Trends Cancer. 5: 233-244. PMID: 30961830
5. Paradoxical dominant negative activity of an immunodeficiency-associated activating PIK3R1 variant.  |  Tomlinson, PR., et al. 2024. bioRxiv.. PMID: 38077044
6. Enhanced STAT3/PIK3R1/mTOR signaling triggers tubular cell inflammation and apoptosis in septic-induced acute kidney injury: implications for therapeutic intervention.  |  Fu, Y., et al. 2024. Clin Sci (Lond). 138: 351-369. PMID: 38411015
7. Somatic Loss-of-Function PIK3R1 and Activating Non-hotspot PIK3CA Mutations Associated with Capillary Malformation with Dilated Veins (CMDV).  |  De Bortoli, M., et al. 2024. J Invest Dermatol. 144: 2066-2077.e6. PMID: 38431221
8. Targeting ERBB2 and PIK3R1 as a therapeutic strategy for dilated cardiomyopathy: A single-cell sequencing and mendelian randomization analysis.  |  He, B., et al. 2024. Heliyon. 10: e25572. PMID: 38434379
9. POU2F1 inhibits miR-29b1/a cluster-mediated suppression of PIK3R1 and PIK3R3 expression to regulate gastric cancer cell invasion and migration.  |  Xiao, Y., et al. 2024. Chin Med J (Engl).. PMID: 39183556
10. Unveiling the role of PIK3R1 in cancer: A comprehensive review of regulatory signaling and therapeutic implications.  |  Gupta, I. and Gaykalova, DA. 2024. Semin Cancer Biol. 106-107: 58-86. PMID: 39197810

The preferred PI 3-kinase p85α antibody is PI 3-kinase p85α Antibody (B-9): sc-1637.