Deficiency of the GPI anchor caused by a somatic mutation of the PIG-A gene in paroxysmal nocturnal hemoglobinuria.

doi:10.1016/0092-8674(93)90250-t

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Article

Deficiency of the GPI anchor caused by a somatic mutation of the PIG-A gene in paroxysmal nocturnal hemoglobinuria.

Cell - 21 May 1993

Takeda J, Miyata T, Kawagoe K, Iida Y, Endo Y, Fujita T, Takahashi M, Kitani T, Kinoshita T

Abstract excerpt

Paroxysmal nocturnal hemoglobinuria is an acquired hematopoietic disease characterized by abnormal blood cell populations in which the biosynthesis of the glycosylphosphatidylinositol (GPI) anchor is deficient. Deficiency of surface expressions of GPI-anchored complement inhibitors leads to compl...

Topics

B-Lymphocytes
Base Sequence
Cell Line
Exons
Glycosylphosphatidylinositols
Hematopoietic Stem Cells
Hemoglobinuria, Paroxysmal
Humans
In Situ Hybridization, Fluorescence
Membrane Proteins
Molecular Sequence Data

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mutation

RNA Splicing

RNA, Messenger

Sequence Deletion

Transfection

X Chromosome

Source

Open in PubMed

Identifiers

PMID: 8500164
DOI: 10.1016/0092-8674(93)90250-t

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-8500164-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

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