DCDC2 belongs to the doublecortin (DCX) superfamily and contains two doublecortin domains. DCDC2 is expressed in fetal and adult CNS.
애플리케이션
Anti-DCDC2 antibody produced in rabbit is suitable for western blot analysis at a working concentration of 1-2μg/mL using a HEK-293T cell lysate expressing human DCDC2.
생화학적/생리학적 작용
DCDC2 is one of the dyslexia susceptibility genes involved in neuronal migration and other developmental processes. The DCX domain of DCDC2 binds tubulin and enhances microtubule polymerization. Several SNPs within the DCDC2 gene have been associated with dyslexia. It modulates neuronal development in the brain.
물리적 형태
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
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Trends in molecular medicine, 12(7), 333-341 (2006-06-20)
Four genes have recently been proposed as candidates for dyslexia: dyslexia susceptibility 1 candidate 1 (DYX1C1), roundabout Drosophila homolog 1 (ROBO1), doublecortin domain-containing protein 2 (DCDC2) and KIAA0319. Each gene is implicated in global brain-development processes such as neural migration
American journal of human genetics, 96(1), 81-92 (2015-01-06)
Nephronophthisis-related ciliopathies (NPHP-RC) are recessive diseases characterized by renal dysplasia or degeneration. We here identify mutations of DCDC2 as causing a renal-hepatic ciliopathy. DCDC2 localizes to the ciliary axoneme and to mitotic spindle fibers in a cell-cycle-dependent manner. Knockdown of
American journal of human genetics, 78(1), 52-62 (2005-12-31)
We searched for linkage disequilibrium (LD) in 137 triads with dyslexia, using markers that span the most-replicated dyslexia susceptibility region on 6p21-p22, and found association between the disease and markers within the VMP/DCDC2/KAAG1 locus. Detailed refinement of the LD region
Proceedings of the National Academy of Sciences of the United States of America, 102(47), 17053-17058 (2005-11-10)
DYX2 on 6p22 is the most replicated reading disability (RD) locus. By saturating a previously identified peak of association with single nucleotide polymorphism markers, we identified a large polymorphic deletion that encodes tandem repeats of putative brain-related transcription factor binding
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