ArticleClinical and experimental immunology2000
Glycosylphosphatidylinositol (GPI)-deficient Jurkat T cells as a model to study functions of GPI-anchored proteins.
Article in Clinical and experimental immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig-a gene Mutation: Support from an in vitro assay based on L5178Y/TkEnvironmental and molecular mutagenesis · 2018Article
- Modulation of natural killer cell functions by interactions between 2B4 and CD48 in cis and in trans.Open biology · 2016Article
- Glycosylphosphatidylinositol-anchored protein deficiency confers resistance to apoptosis in PNH.Experimental hematology · 2009Article
- The glycosylphosphatidylinositol anchor: a complex membrane-anchoring structure for proteins.Biochemistry · 2008Review
- A chemical approach to unraveling the biological function of the glycosylphosphatidylinositol anchor.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Relationship between aplastic anemia and paroxysmal nocturnal hemoglobinuria.International journal of hematology · 2002Review
- Glycosylphosphatidylinositol Anchor Deficiency Attenuates the Production of Infectious HIV-1 and Renders Virions Sensitive to Complement Attack.AIDS research and human retrovirusesArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many cell surface proteins attached to the membrane by GPI are involved in cell signalling. However, the role of the GPI membrane anchor itself remains poorly understood. GPI-defective cells from patients with paroxysmal nocturnal haemoglobinuria (PNH) are relatively resistant to apoptosis induction. We developed a Jurkat T cell model for GPI deficiency by isolating a GPI-negative mutant, which is defective in the GPI biosynthetic gene PIG-A. Using retroviral PIG-A gene transfer along with the transfer of a vector control, we obtained two genetically identical cell lines, distinguished only by expression of the PIG-A gene and, thus, their ability to produce GPI. Cell proliferation and survival were not affected by this difference. Apoptotic stimuli such as serum starvation and camptothecin exposure elicited similar responses. In contrast, GPI-defective Jurkat cells were more susceptible to Fas-mediated apoptosis than GPI-positive cells. These results indicate that a deficiency in GPI-anchored proteins, as is found in PNH, does not confer resistance to apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.