07-888
Anti-phospho-PRAS40 (Thr246) (Proline-Rich AKT substrate) Antibody
Upstate®, from rabbit
Synonym(s):
40 kDa proline-rich AKT substrate, AKT1 substrate 1 (proline-rich), proline-rich Akt substrate, 40 kDa
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
species reactivity
mouse, human
manufacturer/tradename
Upstate®
technique(s)
western blot: suitable
isotype
IgG
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
phosphorylation (pThr246)
Gene Information
human ... AKT1S1(84335)
mouse ... Akt1S1(67605)
General description
PRAS40 (Proline Rich Akt Substrate, 40 kDa), also known as AKT1S1, is a ubiquitously express protein that is phosphorylated on residue Thr246 via the PI3K/Akt pathway. It was originally discovered as an Akt substrate as it has the putative Akt phosphorylation motif of RxRxxpS/pT2. This phosphorylation allows it to bind 14-3-3 and Raptor of the mTOR complex mTORC1. PRAS40 is known to bind to and regulate mTORC1 (mTOR, Raptor, mLST8) kinases activity that is activated by insulin downstream of PI3K and Akt and subsequently phosphorylates p70S6K and 4EBP1. PRAS40 is known to have a putative TOS motif (FVMDE) that allows it bind to Raptor of mTORC1 in the absence of insulin1. It is thought that through it binding to the Raptor, PRAS40 inhibits the kinase activity of mTORC1 by preventing to bind to its substrates such as p70S6K and 4EBP1.
Specificity
Recognizes phosphorylated PRAS40 (Thr246)), Mr 40 kDa.
Immunogen
Peptide corresponding to amino acid region encompassing the human phospho-PRAS40 (Thr246).
Application
Anti-phospho-PRAS40 (Thr246) (Proline-Rich AKT substrate) Antibody is an antibody against phospho-PRAS40 (Thr246) for use in WB.
Immunoblot Analysis: A 1:1000 dilution of this lot detected phosphorylated PRAS40 (Thr246) in RIPA lysates of unstimulated and PDGF stimulated NIH3T3 cells.
Quality
Routinely evaluated by Western Blot on PDGF stimulated NIH3T3 cell lysates.
Western Blot Analysis:
A 1:1000 dilution of this lot detected phosphorylated PRAS40 (Thr246) in RIPA lysates of unstimulated and PDGF stimulated NIH3T3 cells.
Western Blot Analysis:
A 1:1000 dilution of this lot detected phosphorylated PRAS40 (Thr246) in RIPA lysates of unstimulated and PDGF stimulated NIH3T3 cells.
Target description
Approx. 40 kDa
Physical form
Format: Purified
Purified rabbit polyclonal IgG in buffer containing PBS (without Mg2+ and Ca2+), pH 7.3 containing 1.0 mg/mL BSA (IgG, protease free) and 0.05% sodium azide and 50% glycerol.
Analysis Note
Control
PDGF stimulated NIH3T3 cells.
PDGF stimulated NIH3T3 cells.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
10 - Combustible liquids
WGK
WGK 2
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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Regulation of Akt during torpor in the hibernating ground squirrel, Ictidomys tridecemlineatus.
McMullen DC, Hallenbeck JM
Journal of Comparative Physiology. B, Biochemical, Systemic, and Environmental Physiology null
Inositol polyphosphate multikinase is a physiologic PI3-kinase that activates Akt/PKB.
Maag, D; Maxwell, MJ; Hardesty, DA; Boucher, KL; Choudhari, N; Hanno, AG; Ma, JF; Snowman et al.
Proceedings of the National Academy of Sciences of the USA null
Paul M Titchenell et al.
Cell metabolism, 23(6), 1154-1166 (2016-05-31)
During insulin-resistant states such as type II diabetes mellitus (T2DM), insulin fails to suppress hepatic glucose production (HGP) yet promotes lipid synthesis. This metabolic state has been termed "selective insulin resistance" to indicate a defect in one arm of the
Anna E Garcia Whitlock et al.
Molecular metabolism, 51, 101246-101246 (2021-05-09)
Stress-induced hyperglycemia is associated with poor outcomes in nearly all critical illnesses. This acute elevation in glucose after injury or illness is associated with increased morbidity and mortality, including multiple organ failure. Stress-induced hyperglycemia is often attributed to insulin resistance
José L Areta et al.
The Journal of physiology, 591(9), 2319-2331 (2013-03-06)
Quantity and timing of protein ingestion are major factors regulating myofibrillar protein synthesis (MPS). However, the effect of specific ingestion patterns on MPS throughout a 12 h period is unknown. We determined how different distributions of protein feeding during 12
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