PRKAB2

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Protein kinase, AMP-activated, beta 2 non-catalytic subunit
Protein PRKAB2 PDB 2f15.png
PDB rendering based on 2f15.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols PRKAB2 ; MGC61468
External IDs OMIM602741 MGI1336185 HomoloGene38046 IUPHAR: 1544 ChEMBL: 2117 GeneCards: PRKAB2 Gene
RNA expression pattern
PBB GE PRKAB2 214474 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 5565 108097
Ensembl ENSG00000131791 ENSMUSG00000038205
UniProt O43741 Q6PAM0
RefSeq (mRNA) NM_005399 NM_182997
RefSeq (protein) NP_005390 NP_892042
Location (UCSC) Chr 1:
147.16 – 147.17 Mb
Chr 3:
97.66 – 97.67 Mb
PubMed search [1] [2]

5'-AMP-activated protein kinase subunit beta-2 is an enzyme that in humans is encoded by the PRKAB2 gene.[1][2]

The protein encoded by this gene is a regulatory 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. This subunit may be a positive regulator of AMPK activity. It is highly expressed in skeletal muscle and thus may have tissue-specific roles.[2]

Related gene problems[edit]

Interactions[edit]

PRKAB2 has been shown to interact with PRKAG2[3] and PRKAG1.[3]

Research on the genes CHD1L and PRKAB2 within lymphoblast cells[4] lead to the conclusion that anomalies appear with the 1q21.1-deletionsyndrome:

  • CHD1L is an enzyme which is involved in untangling the chromatides and the DNA repair system. With 1q21.1 deletion syndrome a disturbance occurs, which leads to increased DNA breaks. The role of CHD1L is similar to that of helicase with the Werner syndrome
  • PRKAB2 is involved in maintaining the energy level of cells. With 1q21.1-deletion syndrome this function was attenuated.

References[edit]

  1. ^ Stapleton D, Mitchelhill KI, Gao G, Widmer J, Michell BJ, Teh T, House CM, Fernandez CS, Cox T, Witters LA, Kemp BE (February 1996). "Mammalian AMP-activated protein kinase subfamily". J Biol Chem 271 (2): 611–4. doi:10.1074/jbc.271.2.611. PMID 8557660. 
  2. ^ a b "Entrez Gene: PRKAB2 protein kinase, AMP-activated, beta 2 non-catalytic subunit". 
  3. ^ a b Cheung, P C; Salt I P; Davies S P; Hardie D G; Carling D (March 2000). "Characterization of AMP-activated protein kinase gamma-subunit isoforms and their role in AMP binding". Biochem. J. (ENGLAND). 346 Pt 3 (3): 659–69. doi:10.1042/0264-6021:3460659. ISSN 0264-6021. PMC 1220898. PMID 10698692. 
  4. ^ Harvard C, Strong E, Mercier E, Colnaghi R, Alcantara D, Chow E, Martell S, Tyson C, Hrynchak M, McGillivray B, Hamilton S, Marles S, Mhanni A, Dawson AJ, Pavlidis P, Qiao Y, Holden JJ, Lewis SM, O'Driscoll M, Rajcan-Separovic E (2011). "Understanding the impact of 1q21.1 copy number variant". Orphanet J Rare Dis 6: 54. doi:10.1186/1750-1172-6-54. PMC 3180300. PMID 21824431. 

Further reading[edit]