DYRK1B

This gene encodes a member of a family of nuclear-localized protein kinases. The encoded protein participates in the regulation of the cell cycle. Expression of this gene may be altered in tumor cells, and mutations in this gene were found to cause abdominal obesity-metabolic syndrome 3. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jun 2014]

Dual Specificity Tyrosine Phosphorylation Regulated Kinase 1B

Dual-specificity kinase which possesses both serine/threonine and tyrosine kinase activities. Enhances the transcriptional activity of TCF1/HNF1A and FOXO1. Inhibits epithelial cell migration. Mediates colon carcinoma cell survival in mitogen-poor environments. Inhibits the SHH and WNT1 pathways, thereby enhancing adipogenesis. In addition, promotes expression of the gluconeogenic enzyme glucose-6-phosphatase catalytic subunit 1 (G6PC1).

Adipose tissue development Source: UniProtKB
Myoblast fusion Source: Ensembl
Peptidyl-serine phosphorylation Source: GO_Central
Peptidyl-threonine phosphorylation Source: GO_Central
Positive regulation of transcription, DNA-templated Source: UniProtKB
Protein autophosphorylation Source: InterPro
Protein phosphorylation Source: UniProtKB

Nucleus

Abdominal obesity-metabolic syndrome 3 (AOMS3):
A form of abdominal obesity-metabolic syndrome, a disorder characterized by abdominal obesity, high triglycerides, low levels of high density lipoprotein cholesterol, high blood pressure, and elevated fasting glucose levels. AOMS3 is characterized by early-onset coronary artery disease, central obesity, hypertension, and diabetes.

Autophosphorylated on tyrosine residues. Phosphorylated by MAP kinase. Tyrosine phosphorylation may be required for dimerization.