Biology:DYRK1B

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Short description: Protein-coding gene in the species Homo sapiens


A representation of the 3D structure of the protein myoglobin showing turquoise α-helices.
Generic protein structure example

Dual specificity tyrosine-phosphorylation-regulated kinase 1B is an enzyme that in humans is encoded by the DYRK1B gene.[1][2]

Function

DYRK1B is a member of the DYRK family of protein kinases. DYRK1B contains a bipartite nuclear localization signal and is found mainly in muscle and testis. The protein is proposed to be involved in the regulation of nuclear functions. Three isoforms of DYRK1B have been identified differing in the presence of two alternatively spliced exons within the catalytic domain.[2]

Interactions

DYRK1B has been shown to interact with:

Clinical significance

One lone missense mutation in Dyrk1B gene (R102C) was found associated with an autosomal dominant early onset Coronary Artery Disease, juvenile-onset truncal obesity, severe hypertension, and type II diabetes mellitus - seen in subjects from a nomadic group in Iran.[5]

See also

References

  1. "Cloning and characterization of DYRK1B, a novel member of the DYRK family of protein kinases". Biochem Biophys Res Commun 254 (2): 474–9. Feb 1999. doi:10.1006/bbrc.1998.9967. PMID 9918863. 
  2. 2.0 2.1 "Entrez Gene: DYRK1B dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1B". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=9149. 
  3. "Mirk protein kinase is activated by MKK3 and functions as a transcriptional activator of HNF1alpha". J. Biol. Chem. 277 (28): 25040–6. Jul 2002. doi:10.1074/jbc.M203257200. PMID 11980910. 
  4. "Serine/threonine kinase Mirk/Dyrk1B is an inhibitor of epithelial cell migration and is negatively regulated by the Met adaptor Ran-binding protein M". J. Biol. Chem. 278 (49): 49573–81. Dec 2003. doi:10.1074/jbc.M307556200. PMID 14500717. 
  5. Keramati AR (2013). "Identification of a Novel Disease Gene for Early Onset Atherosclerosis, Diabetes and Metabolic Syndrome by Whole Exome Sequencing and Linkage Analysis". Circulation 128 (22 Supplement). http://circ.ahajournals.org/cgi/content/meeting_abstract/128/22_MeetingAbstracts/A15938. 

Further reading