Basic Information

Symbol
PRKAA2
RNA class
mRNA
Alias
Protein Kinase AMP-Activated Catalytic Subunit Alpha 2 AMPK AMPKa2 5'-AMP-Activated Protein Kinase Catalytic Subunit Alpha-2 Protein Kinase, AMP-Activated, Alpha 2 Catalytic Subunit Hydroxymethylglutaryl-CoA Reductase Kinase Acetyl-CoA Carboxylase Kinase AMPK Subunit Alpha-2 ACACA Kinase HMGCR Kinase EC 2.7.11.1 AMPK2 PRKAA 5'-AMP-Activated Protein Kinase, Catalytic Alpha-2 Chain AMPK-Alpha-2 Chain AMPK Alpha 2 EC 2.7.11.31 EC 2.7.11
Location (GRCh38)
Forensic tag(s)
Wound age identification

MANE select

Transcript ID
NM_006252.4
Sequence length
9355.0 nt
GC content
0.3522

Secondary Structure

Generated by RNAfold
Minimum free energy (MFE) structure:
Secondary structure that contributes a minimum of free energy.
Ensemble properties:
Thermodynamic properties of the Boltzmann ensemble.
Minimum free energy
- kcal/mol
MFE Structure Visualization
Structure Prediction
MFE Structure Prediction
-

Transcripts

ID Sequence Length GC content
GCACUGUGGGUAGGCGGCGGCGGCGGCGGCUACGCGGAGCGGCAGGCGG… 9355 nt 0.3522
Summary

The protein encoded by this gene is a catalytic subunit of the AMP-activated protein kinase (AMPK). AMPK is a heterotrimer consisting of an alpha catalytic subunit, and non-catalytic beta and gamma subunits. AMPK is an important energy-sensing enzyme that monitors cellular energy status. In response to cellular metabolic stresses, AMPK is activated, and thus phosphorylates and inactivates acetyl-CoA carboxylase (ACC) and beta-hydroxy beta-methylglutaryl-CoA reductase (HMGCR), key enzymes involved in regulating de novo biosynthesis of fatty acid and cholesterol. Studies of the mouse counterpart suggest that this catalytic subunit may control whole-body insulin sensitivity and is necessary for maintaining myocardial energy homeostasis during ischemia. [provided by RefSeq, Jul 2008] CIViC Summary for PRKAA2 Gene

Forensic Context

A study in human patients demonstrated that the PRKAA2 is associated with cell motility and re-epithelialization during wound healing, where a hypoxic environment can downregulate its activity to induce downstream mTORC1 target expression [Wu et al. DOI:10.21037/atm-22-2033].