DYRK1A


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DYRK1A

A gene on chromosome 21q22.13 that encodes a member of the dual-specificity tyrosine-phosphorylation-regulated kinase (DYRK) family, which catalyses its autophosphorylation on serine/threonine and tyrosine residues. DYRK1A may play a key role in a signalling pathway that regulates cell proliferation and may be involved in brain development. 

Molecular pathology
DYRK1A is a candidate gene for learning defects associated with Down syndrome.
References in periodicals archive ?
The resultant publication entitled, "Epigallocatechin-3-gallate, a DYRK1A inhibitor, rescues cognitive deficits in Down syndrome mouse models and in humans" was published in the journal Molecular Nutrition & Food Research.
The study aimed to investigate the potential benefits of normalizing the activity of the kinase, DYRK1A, which is overexpressed in Down syndrome.
In Ts65Dn mice, green tea extract (Epi-Gallo-Catechin Gallate/EGCG) blocked the harmful effects of DYRK1A and restored normal physiology, learning, and behavior.
Green tea polyphenols rescue of brain defects induced by overexpression of DYRK1A.
pl-carboline compounds, including harmine, inhibit DYRK1A and tau phosphorylation at multiple Alzheimer's disease-related sites.
Other innovative projects currently in development include SEL141, an early stage discovery program of DYRK1A kinase inhibitors with therapeutic potential in the treatment targeting Alzheimer's disease and Down syndrome, SEL201-novel small molecule MNK1/2 inhibitors in oncology, cancer metabolism platform and inflammasome platform.
DYRK1A phosphorylates NFAT, thereby mediating its nuclear export (27).
Two key genes closely implicated with the neuropathological characteristics in Down syndrome: DYRK1A and RCAN1.
One of these alkaloids, called harmine, inhibits a protein known as DYRK1A, which has been implicated by this and other studies in the formation of tau phosphorylation.
Pharmacological inhibition of DYRK1A through the use of beta-carboline alkaloids may provide an opportunity to intervene therapeutically to alter the onset or progression of tau pathology in Alzheimer's disease," Dr.
DYRK1A might control proliferation and maturation events during development (Miyata and Nishida, 1999).
Three proteins EIF2AK2, DYRK1A and AKAP13 have been found to cause a malfunction in tau, a protein critical to the formation of the microtubule bridges within brain cells, or neurons.