AV53846
Anti-PRKAA1 antibody produced in rabbit
affinity isolated antibody
Synonym(e):
Anti-AMPK, Anti-AMPKa1, Anti-MGC33776, Anti-MGC57364, Anti-Protein kinase, AMP-activated, α 1 catalytic subunit
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Alle Fotos(2)
About This Item
UNSPSC-Code:
12352203
Biologische Quelle
rabbit
Konjugat
unconjugated
Antikörperform
affinity isolated antibody
Antikörper-Produkttyp
primary antibodies
Klon
polyclonal
Form
buffered aqueous solution
Mol-Gew.
62 kDa
Speziesreaktivität
human
Konzentration
0.5 mg - 1 mg/mL
Methode(n)
immunohistochemistry: suitable
western blot: suitable
NCBI-Hinterlegungsnummer
UniProt-Hinterlegungsnummer
Versandbedingung
wet ice
Lagertemp.
−20°C
Posttranslationale Modifikation Target
unmodified
Angaben zum Gen
human ... PRKAA1(5562)
Allgemeine Beschreibung
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.
Immunogen
Synthetic peptide directed towards the N terminal region of human PRKAA1
Anwendung
Anti-PRKAA1 antibody produced in rabbit is suitable for western blotting at a concentration of 1μg/mL.
Biochem./physiol. Wirkung
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.
Sequenz
Synthetic peptide located within the following region: GELFDYICKNGRKSDVPGVVKTGSTKELDEKESRRLFQQILSGVDYCHRH
Physikalische Form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
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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Preisangaben
Lagerklassenschlüssel
12 - Non Combustible Liquids
WGK
WGK 3
Flammpunkt (°F)
Not applicable
Flammpunkt (°C)
Not applicable
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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
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
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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