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Merck
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主要文件

AV53846

Sigma-Aldrich

Anti-PRKAA1 antibody produced in rabbit

affinity isolated antibody

别名:

Anti-AMPK, Anti-AMPKa1, Anti-MGC33776, Anti-MGC57364, Anti-Protein kinase, AMP-activated, α 1 catalytic subunit

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About This Item

UNSPSC代码:
12352203

生物来源

rabbit

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

buffered aqueous solution

分子量

62 kDa

种属反应性

human

浓度

0.5 mg - 1 mg/mL

技术

immunohistochemistry: suitable
western blot: suitable

NCBI登记号

UniProt登记号

运输

wet ice

储存温度

−20°C

靶向翻译后修饰

unmodified

基因信息

human ... PRKAA1(5562)

一般描述

PRKAA1 gene encodes the catalytic α-subunit of 5′ AMP-activated protein kinase (AMPK) that belongs to ser/thr protein kinase family and is localized both in the cytoplasm and in the nucleus. AMPK is a heterotrimeric complex consists of a catalytic α subunit and regulatory β and γ subunits.

免疫原

Synthetic peptide directed towards the N terminal region of human PRKAA1

应用

Anti-PRKAA1 antibody produced in rabbit is suitable for western blotting at a concentration of 1μg/mL.

生化/生理作用

AMPK is a cellular energy sensor present in all eukaryotic cells. It is stimulated by high AMP and low ATP concentration and regulates the activities of a number of key metabolic enzymes through allosteric mechanism. Increasing concentrations of AMP during the energy shortage stimulates phosphorylation by an upstream protein kinase and inhibits dephosphorylation, resulting in activation of catabolic pathways and switching off of ATP-consuming biosynthetic pathways. PRKAA1 also facilitates the autophagy-mediated damaged mitochondria clearance for erythrocyte maturation and homeostasis. Additionally, AMPK phosphorylates TSC2 to protect cells from energy deprivation-induced apoptosis and regulates cell growth and survival.

序列

Synthetic peptide located within the following region: GELFDYICKNGRKSDVPGVVKTGSTKELDEKESRRLFQQILSGVDYCHRH

外形

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

免责声明

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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储存分类代码

12 - Non Combustible Liquids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Elżbieta Sarnowska et al.
Postepy higieny i medycyny doswiadczalnej (Online), 67, 750-760 (2013-09-11)
AMP-activated protein kinase (AMPK) is one of the major energy sensor at both: cellular and whole body level. It exists as heterotrimer containing three subunits: the catalytic α subunit, β and regulatory γ. AMPK is localized both in the cytoplasm
Sukriti Krishan et al.
Journal of clinical pathology, 67(9), 758-763 (2014-06-05)
The PRKAA1 gene encodes the catalytic α-subunit of 5′ AMP-activated protein kinase (AMPK). AMPK is a cellular energy sensor that maintains energy homeostasis within the cell and is activated when the AMP/ATP ratio increases. When activated, AMPK increases catabolic processes
Ken Inoki et al.
Cell, 115(5), 577-590 (2003-12-04)
Mutations in either the TSC1 or TSC2 tumor suppressor gene are responsible for Tuberous Sclerosis Complex. The gene products of TSC1 and TSC2 form a functional complex and inhibit the phosphorylation of S6K and 4EBP1, two key regulators of translation.
Huaiping Zhu et al.
Autophagy, 10(9), 1522-1534 (2014-07-06)
AMP-activated protein kinase α1 knockout (prkaa1(-/-)) mice manifest splenomegaly and anemia. The underlying molecular mechanisms, however, remain to be established. In this study, we tested the hypothesis that defective autophagy-dependent mitochondrial clearance in prkaa1(-/-) mice exacerbates oxidative stress, thereby enhancing
Abubakar Wani et al.
Autophagy, 17(11), 3813-3832 (2021-01-07)
Alzheimer disease (AD) is usually accompanied by two prominent pathological features, cerebral accumulation of amyloid-β (Aβ) plaques and presence of MAPT/tau neurofibrillary tangles. Dysregulated clearance of Aβ largely contributes to its accumulation and plaque formation in the brain. Macroautophagy/autophagy is

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