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Merck
CN

SAB4200256

Anti-AKT1S1 antibody, Mouse monoclonal

clone AKT1S1-3, purified from hybridoma cell culture

别名:

Monoclonal Anti-AKT1 substrate 1 (proline-rich), Monoclonal Anti-Lobe, Monoclonal Anti-PRAS40, Monoclonal Anti-PROLINE-RICH AKT SUBSTRATE, 40-KD

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关于此项目

NACRES:
NA.44
UNSPSC Code:
12352203
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产品名称

Anti-AKT1S1 antibody, Mouse monoclonal, clone AKT1S1-3, purified from hybridoma cell culture

biological source

mouse

conjugate

unconjugated

antibody form

purified from hybridoma cell culture

antibody product type

primary antibodies

clone

AKT1S1-3, monoclonal

form

buffered aqueous solution

mol wt

antigen ~40 kDa

species reactivity

human

concentration

~1.0 mg/mL

technique(s)

immunoprecipitation (IP): suitable
western blot: 2-8 μg/mL using whole extracts of human MDA-MB-231cells.

isotype

IgG1

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... AKT1S1(84335)

Application

Monoclonal Anti-AKT1S1 antibody is suitable for use in western blot (2-8 μg/mL using whole extracts of human MDA-MB-231cells) and immunoprecipitation.

Biochem/physiol Actions

Akt1 substrate 1 (AKT1S1) is involved in the PI3KAkt/ protein kinase B (PKB) survival pathway. Phosphorylation of AKT1S1 by Akt and mammalian target of rapamycin complex 1 (mTORC1) disrupts the binding between mTORC1 and AKT1S1, relieves the inhibitory effect of AKT1S1 on mTORC1 activity, and leads to the binding of AKT1S1 to 14-3-3, a cytosolic anchor protein. The binding of AKT1S1 to 14-3-3 requires amino acids and insulin, which is partially inhibited by rapamycin.

General description

AKT1S1 is a raptor-associated protein that interacts with mTORC1 and subsequently inhibits the mTORC1 signaling pathway. This raptor-binding protein also inhibits phosphorylation of S6K1 and cell growth. Expression of AKT1S1 has been implicated in breast and pulmonary carcinogenesis, as well as in mediating insulin sensitivity . Monoclonal Anti-AKT1S1 antibody is specific for human AKT1S1 (approx. 40 kDa).
Monoclonal Anti-AKT1S1 (mouse IgG1 isotype) is derived from the hybridoma AKT1S1-3 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a fusion protein corresponding to the N-terminus of human AKT1S1. Akt1 substrate 1 (AKT1S1) is also named as proline-rich Akt-substrate of 40 kDa (PRAS40). The rapamycin-sensitive mammalian target of rapamycin complex 1 (mTORC1) consists of mTOR, raptor, mLST8 and AKT1S1, that controls protein translation. AKT1S1 contains a TOR signaling (TOS) motif that mediates its binding to mTORC1.

Immunogen

The corresponding sequence differs by a single amino acid in rat, and by 2 amino acids in mouse AKT1S1.
fusion protein corresponding to the N-terminus of human AKT1S1.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

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存储类别

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

常规特殊物品
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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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PRAS40 regulates mTORC1 kinase activity by functioning as a direct inhibitor of substrate binding
Wang L, et al.
Test, 282(27), 20036-20044 (2007)
PRAS40 is a target for mammalian target of rapamycin complex 1 and is required for signaling downstream of this complex
Fonseca BD, et al.
Test, 282(34), 24514-24524 (2007)
Emilie Vander Haar et al.
Nature cell biology, 9(3), 316-323 (2007-02-06)
Insulin stimulates protein synthesis and cell growth by activation of the protein kinases Akt (also known as protein kinase B, PKB) and mammalian target of rapamycin (mTOR). It was reported that Akt activates mTOR by phosphorylation and inhibition of tuberous
Role of PRAS40 in Akt and mTOR signaling in health and disease
Wiza C, et al.
American Journal of Physiology. Endocrinology and Metabolism, 302(12), E1453-E1460 (2012)
Yasemin Sancak et al.
Molecular cell, 25(6), 903-915 (2007-03-28)
The heterotrimeric mTORC1 protein kinase nucleates a signaling network that promotes cell growth in response to insulin and becomes constitutively active in cells missing the TSC1 or TSC2 tumor suppressors. Insulin stimulates the phosphorylation of S6K1, an mTORC1 substrate, but

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