Target intelligence / Profile preview

Nuclear distribution protein nudE homolog 1 (NDE1)

Target
NDE1
Molecular classification
Other (Cytoskeletal-associated scaffold/adaptor protein, Centrosomal protein)
01

Overview

Nuclear distribution protein nudE homolog 1 (NDE1) is a centrosomal scaffold/adaptor protein vital for neurodevelopment, especially cortical brain formation. It governs centrosome duplication, mitotic spindle formation, and the organization and orientation of microtubules during cell division, particularly in neural progenitors[1][3][5]. By controlling the axis of cell division, it influences the balance between neural progenitor expansion and differentiation, affecting total neuron numbers and cortical layering[1][3][5]. NDE1 interacts with LIS1 and dynein to regulate nuclear migration and mitotic spindle formation, and with chromatin modifiers to safeguard genome integrity during S phase, preventing DNA damage in developing neurons[2][4][5]. Loss-of-function mutations in both alleles cause severe developmental brain disorders such as lissencephaly with microcephaly, while heterozygous loss may raise cancer risk[2][3]. NDE1 is not currently considered a classical drug target (receptor, enzyme, transporter), but is instead a key player in cell architecture and genome safeguarding during neurodevelopment[1][3][5].

Other names
NDE1NUDENudEFLJ20101NDEHOM-TES-87LIS4MHACNUDE1LIS1-interacting protein NUDE1
02

Biological functions

Cell cycle progressionMitosisCentrosome duplicationMicrotubule organizationNeuronal migrationRegulation of mitotic spindle orientationNuclear migrationGenomic stability maintenanceNegative regulation of ciliogenesis
03

Disease associations

Neurodevelopmental disease (Lissencephaly 4, Microhydranencephaly, congenital microcephaly, microlissencephaly)Cancer (implicated as a risk factor)Possibly other brain developmental disorders
04

Safety considerations

Mutations cause severe congenital brain malformations (lissencephaly, microcephaly, brain atrophy)Loss of function can result in catastrophic genomic instability and apoptosis in neural progenitors

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