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Key Documents

PLA0238

Sigma-Aldrich

Rabbit anti-AKT1 Antibody, Affinity Purified

Powered by Bethyl Laboratories, Inc.

Synonym(e):

AKT, AKT1m, CWS6, PKB, PKB alpha, PKB-ALPHA, PRKBA, Protein kinase B, RAC, RAC-ALPHA, RAC-PK-alpha, protein kinase B alpha, proto-oncogene c-Akt, rac protein kinase alpha, serine-threonine protein kinase, v-akt murine thymoma viral oncogene homolog 1, v-akt murine thymoma viral oncogene-like protein 1

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About This Item

UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

rabbit

Qualitätsniveau

100

Antikörperform

affinity purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Qualität

Powered by Bethyl Laboratories, Inc.

Speziesreaktivität

human

Methode(n)

immunohistochemistry: 1:500-1:2,000
western blot: 1:2,000- 1:10,000

Hinterlegungsnummer

NP_005154.1

UniProt-Hinterlegungsnummer

P31749

Versandbedingung

wet ice

Lagertemp.

2-8°C

Angaben zum Gen

rabbit ... AKT1(207)

Immunogen

The epitope recognized by PLA0238 maps to a region between residue 25 and 75 of human v-akt murine thymoma viral oncogene homolog 1 using the numbering given in entry NP_005154.1 (GeneID 207).

Physikalische Form

Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% Sodium Azide

Sonstige Hinweise

AKT1 is a serine-threonine kinase that functions downstream of PI-3 kinase and is known to phosphorylate several proteins. AKT1 mediates the effects of several growth factors such as insulin, IGF-1, EGF, and PDGF to control cell survival and apoptosis. There are numerous substrates of AKT1, some of which are: GSK3-alpha and beta, mTOR, TSC2, Bad, c-Raf, and caspase 9.

Haftungsausschluss

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.

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Lagerklassenschlüssel

12 - Non Combustible Liquids

WGK

nwg

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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Die Dokumentenbibliothek aufrufen

Hua-Yu Zhu et al.
PloS one, 9(5), e97114-e97114 (2014-05-13)
As an important oncogenic miRNA, microRNA-21 (miR-21) is associated with various malignant diseases. However, the precise biological function of miR-21 and its molecular mechanism in hypertrophic scar fibroblast cells has not been fully elucidated. Quantitative Real-Time PCR (qRT-PCR) analysis revealed
Xiaoyun Tang et al.
Journal of lipid research, 55(11), 2389-2400 (2014-09-12)
Lipid phosphate phosphatase-1 (LPP1) degrades lysophosphatidate (LPA) and attenuates receptor-mediated signaling. LPP1 expression is low in many cancer cells and tumors compared with normal tissues. It was hypothesized from studies with cultured cells that increasing LPP1 activity would decrease tumor
Tetsuo Mashima et al.
Cancer research, 74(17), 4888-4897 (2014-06-26)
Endocrine therapy is the standard treatment for advanced prostate cancer; however, relapse occurs in most patients with few treatment options available after recurrence. To overcome this therapeutic hurdle, the identification of new molecular targets is a critical issue. The capability
Mariëtte E G Kranendonk et al.
Obesity (Silver Spring, Md.), 22(10), 2216-2223 (2014-07-22)
Insulin resistance (IR) is a key mechanism in obesity-induced cardiovascular disease. To unravel mechanisms whereby human adipose tissue (AT) contributes to systemic IR, the effect of human AT-extracellular vesicles (EVs) on insulin signaling in liver and muscle cells was determined.
Makoto Kurano et al.
Biochimica et biophysica acta, 1841(9), 1217-1226 (2014-05-13)
High-density lipoprotein (HDL) has been proposed to enhance β-cell functions. Clinical studies have suggested that apolipoprotein M (apoM), which rides mainly on HDL, is involved in diabetes; however, the underlying mechanism has not yet been elucidated. Recently, apoM was shown
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