Phospho-PKA alpha/beta/gamma (Thr197) Rabbit Polyclonal Antibody

Phospho-PKA alpha/beta/gamma (Thr197) Rabbit Polyclonal Antibody

Size1:50μl Price1:$168
Size2:100μl Price2:$300
Size3:500μl Price3:$1200
SKU: APRab00837 Category: Polyclonal Antibody Tags: , , , , , ,

Datasheet

Summary

Production Name

Phospho-PKA alpha/beta/gamma (Thr197) Rabbit Polyclonal Antibody

Description

Primary antibody

Host

Rabbit

Application

WB,IHC,IHC,ICC/IF,ELISA

Reactivity

Human,Mouse,Rat

 

Performance

Conjugation

Unconjugated

Modification

Phosphorylated

Isotype

IgG

Clonality

Polyclonal Antibody

Form

Liquid

Storage

Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.

Buffer

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide, pH 7.3.

Purification

Affinity Chromatography

 

Immunogen

Gene Name

PRKACA/PRKACB/PRKACG

Alternative Names

PRKACA; PKACA; cAMP-dependent protein kinase catalytic subunit alpha; PKA C-alpha; PRKACB; cAMP-dependent protein kinase catalytic subunit beta; PKA C-beta; PRKACG; cAMP-dependent protein kinase catalytic subunit gamma; PKA C-gamma

Gene ID

5566/5567

SwissProt ID

P17612/P22694/P22612

 

Application

Dilution Ratio

WB: 1/500-1/1000 IHC: 1/50-1/100 IF: 1/50-1/200 ELISA: 1/10000

Molecular Weight

Calculated MW: 40 kDa; Observed MW: 40 kDa

 

Background

PRKACA (protein kinase cAMP-activated catalytic subunit alpha) encodes one of the catalytic subunits of protein kinase A, which exists as a tetrameric holoenzyme with two regulatory subunits and two catalytic subunits, in its inactive form. cAMP causes the dissociation of the inactive holoenzyme into a dimer of regulatory subunits bound to four cAMP and two free monomeric catalytic subunits. Four different regulatory subunits and three catalytic subunits have been identified in humans. cAMP-dependent phosphorylation of proteins by protein kinase A is important to many cellular processes, including differentiation, proliferation, and apoptosis. Constitutive activation of this gene caused either by somatic mutations, or genomic duplications of regions that include this gene, have been associated with hyperplasias and adenomas of the adrenal cortex and are linked to corticotropin-independent Cushing's syndrome. Alternative splicing results in multiple transcript variants encoding different isoforms. Tissue-specific isoforms that differ at the N-terminus have been described, and these isoforms may differ in the post-translational modifications that occur at the N-terminus of some isoforms.

 

Research Area

Signal Transduction