Anti-PI3-kinase p85-α antibody detects endogenous levels of total PI3-kinase p85-α protein.
The PIK3R1 (phosphoinositide-3-kinase regulatory subunit 1) gene is mapped to human chromosome 5q13.1. It encodes for p85α regulatory subunit.
Immunogen
The antiserum was produced against synthesized peptide derived from human PI3-kinase p85-alpha/gamma.
Immunogen Range: 436-485
Application
Anti-PI3-kinase p85-α antibody produced in rabbit has been used in western blotting.
Biochem/physiol Actions
PIK3R1 (phosphoinositide-3-kinase regulatory subunit 1) is known to mediate immune cell differentiation, development and function. Dominant mutations of PIK3R1 causes hyperactivation of the PI3K signaling pathway, leading to immunodeficiency and also SHORT syndrome (short stature, hyperextensibility, hernia, ocular depression, Rieger anomaly, and teething delay). PI3K is an important part of insulin and growth factor signaling. PIK3R1 gene is considered to be intolerant to functional variation among the human population. In human, downregulation of PIK3R1 is observed in many types of cancer. PIK3R1 is regarded as a tumor suppressor gene. PIK3R1 mediates tumorigenesis and malignant progression. The gene harbors receptor tyrosine kinases activity and participates in the activation of class IA PI3Ks.
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
G-protein-coupled receptor (GPCR)-related proteins are dysregulated and the GPCR CC-chemokine receptor 10 (CCR10) is significantly upregulated in inflammation-driven HCC. However, CCR10's role in inflammation-driven hepatocarcinogenesis remains unknown. The aim of this study was to evaluate the role of CCR10 in
Iris Malformation and Anterior Segment Dysgenesis in Mice and Humans With a Mutation in PI 3-Kinase.
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