DYRK

DYRK

DYRK (dual-specificity tyrosine-regulated kinases) are an evolutionary conserved family of protein kinases. The DYRK family is formed by three subfamilies: the DYRK subfamily, the homeodomain-interacting kinases (HIPKs), and the pre-messenger RNA-processing protein 4 kinases (PRP4Ks). The DYRK subfamily contains five members in humans that are clustered into two classes based on their phylogenetic relationships: class I DYRKs, DYRK1A and DYRK1B (also known as Mirk from minibrain-related kinase) and class II DYRKs, DYRK2, DYRK3 (also known as REDK from regulatory erythroid kinase) and DYRK4. DYRKs are pleiotropic factors that phosphorylate a broad set of proteins involved in many different cellular processes. These include factors that have been associated with all the hallmarks of cancer, from genomic instability to increased proliferation and resistance, programmed cell death, or signaling pathways whose dysfunction is relevant to tumor onset and progression.

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More About DYRK

DYRK (dual-specificity tyrosine-regulated kinases) are an evolutionary conserved family of protein kinases. The DYRK family is formed by three subfamilies: the DYRK subfamily, the homeodomain-interacting kinases (HIPKs), and the pre-messenger RNA-processing protein 4 kinases (PRP4Ks). The DYRK subfamily contains five members in humans that are clustered into two classes based on their phylogenetic relationships: class I DYRKs, DYRK1A and DYRK1B (also known as Mirk from minibrain-related kinase) and class II DYRKs, DYRK2, DYRK3 (also known as REDK from regulatory erythroid kinase) and DYRK4. DYRKs are pleiotropic factors that phosphorylate a broad set of proteins involved in many different cellular processes. These include factors that have been associated with all the hallmarks of cancer, from genomic instability to increased proliferation and resistance, programmed cell death, or signaling pathways whose dysfunction is relevant to tumor onset and progression.[1]


[1] J Boni et al. The DYRK Family of Kinases in Cancer: Molecular Functions and Therapeutic Opportunities. Cancers (Basel). 2020 Jul 29;12(8):2106.

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