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NDE1 encodes a member of the nuclear distribution E (NudE) family of proteins.
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Interaction between NDE1 and high birth weight was associated with increased susceptibility to schizophrenia.
study strengthens the evidence for association between rare variants within NDE1 and schizophrenia, and may shed light into the molecular mechanisms underlying this severe psychiatric disorder.
These data show that cell cycle-dependent mechanisms can control ciliary length through a CDK5-FBW7-NDE1 pathway.
study provided comprehensive documentation of the expression patterns of Nde1 and Ndel1 (show NDEL1 Antibodies) in cultured cells as well as in mouse and human brains, and also highlighting that dosage effects of these two proteins might contribute to some cases of mental disorder
Description of a severe microcephaly syndrome where an autosomal recessive condition combines an inherited segmental duplication mediated deletion with a mutation in the NDE1 gene within the non-deleted homolog.
In three related patients with microhydranencephaly, a homozygous deletion that encompasses NDE1 exon 2 containing the initiation codon was identified.
analysis of mixed NDE1-NDEL1 (show NDEL1 Antibodies) complexes demonstrates that NDE1 and NDEL1 (show NDEL1 Antibodies) can interact directly.
Mutually exclusive cytoplasmic dynein (show DYNC1H1 Antibodies) regulation by NudE-Lis1 (show PAFAH1B1 Antibodies) and dynactin (show DCTN1 Antibodies).
NDE1 mutations cause a severe microlissencephaly syndrome. Patient's NDE1 proteins are unstable, cannot bind cytoplasmic dynein (show DYNC1H1 Antibodies), and do not localize properly to the centrosome.
NDE1 deficiency causes both a severe failure of neurogenesis and a deficiency in cortical lamination
This gene encodes a member of the nuclear distribution E (NudE) family of proteins. The encoded protein is localized at the centrosome and interacts with other centrosome components as part of a multiprotein complex that regulates dynein function. This protein plays an essential role in microtubule organization, mitosis and neuronal migration. Mutations in this gene cause lissencephaly 4, a disorder characterized by lissencephaly, severe brain atrophy, microcephaly, and severe mental retardation. Alternative splicing results in multiple transcript variants.
LIS1-interacting protein NUDE1, rat homolog
, nuclear distribution protein nudE homolog 1
, nudE nuclear distribution E homolog 1
, nudE nuclear distribution gene E homolog 1