lissencephaly/proline

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LIS1 and XLIS (DCX) mutations cause most classical lissencephaly, but different patterns of malformation.

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Ingia / Ingia

Classical lissencephaly (LIS) is a neuronal migration disorder resulting in brain malformation, epilepsy and mental retardation. Deletions or mutations of LIS1 on 17p13.3 and mutations in XLIS ( DCX ) on Xq22.3-q23 produce LIS. Direct DNA sequencing of LIS1 and XLIS was performed in 25 children with

Armadillo Repeat Containing 8alpha Binds to HRS and Promotes HRS Interaction with Ubiquitinated Proteins.

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Ingia / Ingia

Recently, we reported that a complex with an essential role in the degradation of Fructose-1,6-bisphosphatase in yeast is well conserved in mammalian cells; we named this mammalian complex C-terminal to the Lissencephaly type-1-like homology (CTLH) complex. Although the function of the CTLH complex

Multisite phosphorylation of doublecortin by cyclin-dependent kinase 5.

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Ingia / Ingia

Doublecortin (DCX) is a 40 kDa microtubule-associated protein required for normal neural migration and cortical layering during development. Mutations in the human DCX gene cause a disruption of cortical neuronal migration. Defects in cdk5 (cyclin-dependent kinase 5) also cause defects in neural

The doublecortin gene family and disorders of neuronal structure.

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Ingia / Ingia

The doublecortin gene family is associated with subcortical band heterotopia, lissencephaly, epilepsy, developmental dyslexia and retinitis pigmentosa. At least 11 genes homologous to the doublecortin gene exist in humans and mice. Cellular processes regulated by different members of the

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Herbal & Natural Medicine

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