Doublecortin-like kinase 2 (DCLK2)

Doublecortin-like kinase 2 (DCLK2) is a serine/threonine protein kinase in the doublecortin family and protein kinase superfamily that contains microtubule-binding domains (N-terminal doublecortin domains) and a C-terminal kinase domain[2][5][1][6]. DCLK2 regulates microtubule polymerization and dendritic morphogenesis independently of its kinase activity and is expressed predominantly in the nervous system from development through adulthood[1][2]. It is involved in the structural plasticity of dendrites and the suppression of synaptic maturation, possibly via phosphorylation-driven signaling pathways[3]. DCLK2 dysfunction is linked to neurodevelopmental disorders and experimental epilepsy phenotypes[2][5]. The protein is structurally similar to DCLK1, a cancer-associated kinase, facilitating comparisons and possible translational interest[4]. DCLK2's kinase activity is regulated through autoregulatory C-terminal tail sequences, with functional roles identified for different splice isoforms[4][6]. No approved drugs directly target DCLK2, but its molecular features may make it a relevant future target in neuroscience and oncology[2][4].

Other names

DCLK2Doublecortin kinase 2Serine/threonine-protein kinase DCLK2

null (no clinically-validated mechanism of action for DCLK2-targeting drugs; for related kinases, inhibition of kinase activity is typical)