Entity Details

Primary name NEXMI_HUMAN
Entity type UniProt
Source Source Link

Details

AccessionQ5QGS0
EntryNameNEXMI_HUMAN
FullNameNeurite extension and migration factor
TaxID9606
Evidenceevidence at transcript level
Length1516
SequenceStatuscomplete
DateCreated2006-10-31
DateModified2021-06-02

Ontological Relatives

GenesNEXMIF

GO terms

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GOName
GO:0001953 negative regulation of cell-matrix adhesion
GO:0005634 nucleus
GO:0005654 nucleoplasm
GO:0005829 cytosol
GO:0007399 nervous system development
GO:0030496 midbody
GO:0033629 negative regulation of cell adhesion mediated by integrin
GO:0072686 mitotic spindle
GO:2000048 negative regulation of cell-cell adhesion mediated by cadherin
GO:2001223 negative regulation of neuron migration

Subcellular Location

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Subcellular Location
Cytoplasm
Nucleus

Domains

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DomainNameCategoryType
IPR032757 Domain of unknown function DUF4683DomainDomain
IPR042794 Neurite extension and migration factorFamilyFamily

Diseases

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Disease IDSourceNameDescription
300912 OMIMMental retardation, X-linked 98 (MRX98)A disorder characterized by significantly below average general intellectual functioning associated with impairments in adaptive behavior and manifested during the developmental period. MRX98 patients show delayed psychomotor development, absent or poor speech development, and postnatal growth retardation, often with microcephaly. Some patients show autistic behavioral features, such as stereotypic hand movements and repetitive behaviors. Additional, more variable features include spasticity, axial hypotonia, seizures, drooling, gastroesophageal reflux, and lack of sphincter control. The disease is caused by variants affecting the gene represented in this entry. A chromosomal aberration involving NEXMIF is found in patients with severe mental retardation. Pericentric inversion inv(X)(p22.3;q13.2) with P2RY8 leading to inactivation of NEXMIF (PubMed:15466006). MRX98 transmission pattern is consistent with X-linked recessive inheritance (PubMed:23615299). In some cases, de novo heterozygous loss-of-function mutations have been found in affected females, while some female carriers are asymptomatic (PubMed:26576034, PubMed:27358180, PubMed:27568816). The female phenotype partially overlaps with the reported male phenotype but includes epilepsy as a relevant feature. The variability of disease manifestation in female carriers is probably due to skewed X inactivation with differential expression in the brain (PubMed:26576034, PubMed:27358180, PubMed:27568816).

Interactions

2 interactions

InteractorPartnerSourcesPublicationsLink
NEXMI_HUMANTERF1_HUMANBioGRID20811636 details
NEXMI_HUMANTERF2_HUMANBioGRID20811636 details