Molecular genetics and molecular biology of dyslexia.
Stockholm, Sweden. In Wiley Interdiscip Rev Cogn Sci, 2011
More importantly, the first genes, some of them found by the study of rare families, have indicated specific neurodevelopmental processes important for the development of dyslexia, including control of neuronal migration for the DYX1C1, DCDC2, and KIAA0319 genes, and a role of axonal and dendritic guidance suggested by the ROBO1 gene.
A theoretical molecular network for dyslexia: integrating available genetic findings.
Nijmegen, Netherlands. In Mol Psychiatry, 2011
We found that 10 of the 14 dyslexia candidate genes (ROBO1, KIAA0319, KIAA0319L, S100B, DOCK4, FMR1, DIP2A, GTF2I, DYX1C1 and DCDC2) fit into a theoretical molecular network involved in neuronal migration and neurite outgrowth.
Progress towards a cellular neurobiology of reading disability.
Easton, United States. In Neurobiol Dis, 2010
In this review we discuss recent findings that revealed neuroanatomic anomalies in RD, studies that identified 3 candidate genes (KIAA0319, DYX1C1, and DCDC2), and compelling evidence that potentially link the function of candidate genes to the neuroanatomic anomalies.
The genetics of reading disability.
Boston, United States. In Curr Psychiatry Rep, 2009
Association studies of positional candidate genes have implicated DCDC2 and KIAA0319 in DYX2, as well as C2ORF3 and MRPL19 (DYX3), whereas DYX1C1/EKN1 (DYX1) and ROBO1 (DYX5) were found to be disrupted by rare translocation breakpoints in reading-disabled individuals.
Seattle, United States. In Unknown Journal, 2000
Pathogenic variants in HPS1, AP3B1 (HPS2), HPS3, HPS4, HPS5, HPS6, DTNBP1 (HPS7), BLOC1S3 (HPS8), and BLOC1S6 (PLDN) are known to cause HPS.