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AKT1S1 Antibody

     
  • 1 - AKT1S1 Antibody ASC11670
    Western blot analysis of AKT1S1 in human brain tissue lysate with AKT1S1 antibody at (A) 1 and (B) 2 µg/mL.
  • 2 - AKT1S1 Antibody ASC11670
    Immunohistochemistry of AKT1S1 in rat brain tissue with AKT1S1 antibody at 2.5 µg/ml.
  • 3 - AKT1S1 Antibody ASC11670
    Immunofluorescence of AKT1S1 in rat brain tissue with AKT1S1 antibody at 20 µg/ml.
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, IF, E, IHC-P
Primary Accession Q96B36
Other Accession NP_115751, 400153980
Reactivity Human, Mouse, Rat
Host Rabbit
Clonality Polyclonal
Isotype IgG
Calculated MW 27383 Da
Concentration (mg/ml) 1 mg/mL
Conjugate Unconjugated
Application Notes AKT1S1 antibody can be used for detection of AKT1S1 by Western blot at 1 - 2 µg/mL.
Additional Information
Gene ID 84335
Other Names Proline-rich AKT1 substrate 1, 40 kDa proline-rich AKT substrate, AKT1S1 {ECO:0000312|EMBL:AAH16043.1}
Target/Specificity AKT1S1; AKT1S1 antibody is human, mouse and rat reactive. At least three isoforms of AKT1S1 are known to exist.
Reconstitution & Storage AKT1S1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year.
PrecautionsAKT1S1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.

For Research Use Only. Not For Use In Diagnostic Procedures.

Protein Information
Name AKT1S1 {ECO:0000312|EMBL:AAH16043.1}
Function Negative regulator of the mechanistic target of rapamycin complex 1 (mTORC1), an evolutionarily conserved central nutrient sensor that stimulates anabolic reactions and macromolecule biosynthesis to promote cellular biomass generation and growth (PubMed:17277771, PubMed:17386266, PubMed:17510057, PubMed:29236692). In absence of insulin and nutrients, AKT1S1 associates with the mTORC1 complex and directly inhibits mTORC1 activity by blocking the MTOR substrate- recruitment site (PubMed:29236692). In response to insulin and nutrients, AKT1S1 dissociates from mTORC1 (PubMed:17386266, PubMed:18372248). Its activity is dependent on its phosphorylation state and binding to 14-3-3 (PubMed:16174443, PubMed:18372248). May also play a role in nerve growth factor-mediated neuroprotection (By similarity).
Cellular Location Cytoplasm, cytosol {ECO:0000250|UniProtKB:Q9D1F4}. Note=Found in the cytosolic fraction of the brain. {ECO:0000250|UniProtKB:Q9D1F4}
Tissue Location Widely expressed with highest levels of expression in liver and heart. Expressed at higher levels in cancer cell lines (e.g. A-549 and HeLa) than in normal cell lines (e.g. HEK293)
Research Areas

BACKGROUND

AKT1S1 Antibody: The Akt signaling pathway contributes to the regulation of apoptosis after a variety of cell death signals. AKT1S1, also known as PRAS40, is a proline-rich substrate of the kinase AKT1 and is thought to play a role in neuroprotection mediated by nerve growth factor (NGF) after transient focal cerebral ischemia (1). AKT1S1 is also a substrate and potential regulator of mammalian target of rapamycin (mTOR), a serine/threonine kinase that regulates cell growth and cell cycle, and a negative regulator of autophagy (2). Treatment with the insulin-like growth factor-1 (IGF1) can indusce the phosphorylation of AKT1S1 via the PI3K/AKT signaling pathway in PC12 cells (3).

REFERENCES

Saito A, Narasimhan P, Hayashi T, et al. Neuroprotective role of a proline-rich Akt substrate in apoptotic neuronal cell death after stroke: relationships with nerve growth factor. J. Neurosci. 2004; 24:1584-93.
Wiza C, Nascimento EB, and Ouwens DM. Role of PRAS40 in Akt and mTOR signaling in health and disease. Am. J. Physiol. Endocrinol. Metab. 2012; 302:E1453-60.
Wang H, Zhang Q, Zhang L, et al. Insulin-like growth factor-1 induces the phosphrylation of PRAS40 via the PI3K/Akt signaling pathway in PC12 cells. Neurosci. Lett. 516:105-9.

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