Akt1 Antibody
This gene encodes the founding member of the Akt serine-threonine protein kinase gene family that also includes Akt2 and Akt3. This kinase is a major downstream effector of the phosphatidylinositol 3-kinase (PI3K) pathway that mediates the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I) . It is activated through recruitment to cellular membranes by PI3K lipid products and by phosphorylation by 3-phosphoinositide dependent kinase-1. It then further phosphorylates different downstream proteins in response to various extracellular signals and thus plays a pivotal role in mediating a variety of cellular processes, such as glucose metabolism, glycogen biosynthesis, protein synthesis and turn over, inflammatory response, cell survival (anti-apoptosis) and development. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Product Specifications
CAS Number
9007-83-4
Specifications
Western blot: 1:1000, IHC (Paraffin) : 1:10-1:50
UniProt
P31750
Host
Rabbit
Reactivity
Mouse
Immunogen
A portion of amino acids 22-49 from the mouse protein was used as the immunogen for this Akt1 antibody.
Clonality
Polyclonal
Isotype
Ig
Applications
WB, IHC, ELISA
Purity
Antigen affinity
Format
Antigen affinity purified
Buffer
In 1X PBS, pH 7.4, with 0.09% sodium azide
Reconstitution
Aliquot the Akt1 antibody and store frozen at -20oC or colder. Avoid repeated freeze-thaw cycles.
Limitations
This Akt1 antibody is available for research use only.
Storage Conditions
Aliquot the Akt1 antibody and store frozen at -20°C or colder. Avoid repeated freeze-thaw cycles.
Formulation
In 1X PBS, pH 7.4, with 0.09% sodium azide
Applications Notes
Titration of the Akt1 antibody may be required due to differences in protocols and secondary/substrate sensitivity.
Prediction Reactivity
Human
Image Legend
Akt1 antibody western blot analysis in mouse heart tissue lysate.
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