Truncated, inactive N-acetylglucosaminyltransferase III (GlcNAc-TIII) induces neurological and other traits absent in mice that lack GlcNAc-TIII.

doi:10.1074/jbc.M202276200

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Article

Truncated, inactive N-acetylglucosaminyltransferase III (GlcNAc-TIII) induces neurological and other traits absent in mice that lack GlcNAc-TIII.

The Journal of biological chemistry - 19 Jul 2002

Bhattacharyya Riddhi, Bhaumik Mantu, Raju T Shantha, Stanley Pamela

Abstract excerpt

N-Acetylglucosaminyltransferase III (GlcNAc-TIII), the product of the Mgat3 gene, transfers the bisecting GlcNAc to the core mannose of complex N-glycans. The addition of this residue is regulated during development and has functional consequences for receptor signaling, cell adhesion, and tumor progression. Mice homozygous for a null mutation at the Mgat3 locus (Mgat3(Delta)) or for a targeted mutation in the...

Topics

Alleles
Animals
Brain
Codon, Nonsense
Female
Gait Disorders, Neurologic
Growth Disorders
Humans
Liver Neoplasms
Male
Mice

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mice, Knockout

N-Acetylglucosaminyltransferases

Nervous System Diseases

Phenotype

Reflex, Abnormal

Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

Source

Open in PubMed

Identifiers

PMID: 11986323
DOI: 10.1074/jbc.M202276200

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 31 Aug 2026.

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