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SAB4502195

Sigma-Aldrich

Anti-PI3-kinase p85-α antibody produced in rabbit

affinity isolated antibody

Synonym(s):

GRB1, P85A, PI3-kinase p85-α subunit, PI3K, PI3K p85-α

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 83 kDa

species reactivity

mouse, rat, human

concentration

~1 mg/mL

technique(s)

ELISA: 1:1000
immunofluorescence: 1:100-1:500
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... PIK3R1(5295)

General description

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

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

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.

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Qiong Wu et al.
Cell death & disease, 9(2), 232-232 (2018-02-16)
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
Aberrant low expression of p85? in stromal fibroblasts promotes breast cancer cell metastasis through exosome-mediated paracrine Wnt10b.
Chen Y
Oncogene, 36(33), 4692-4705 (2017)
Oncogenic mutations in GNAQ occur early in uveal melanoma.
Onken MD
Investigative Ophthalmology & Visual Science, 49(12), 5230-5234 (2008)
Dominant Splice Site Mutations in PIK3R1 Cause Hyper IgM Syndrome, Lymphadenopathy and Short Stature.
Petrovski S
Journal of clinical immunology, 36(5), 462-471 (2016)
?-Arrestin1 enhances hepatocellular carcinogenesis through inflammation-mediated Akt signalling.
Yang Y
Nature Communications, 6:7369 (2015)

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