ArticleSmall GTPases2011
Gimap3: A foot-in-the-door to tissue-specific regulation of mitochondrial DNA genetics.
Article in Small GTPases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- The GIMAP Family Proteins: An Incomplete Puzzle.Frontiers in immunology · 2021Review
- Mitochondrial maintenance failure in aging and role of sexual dimorphism.Archives of biochemistry and biophysics · 2015Review
- Tubulin- and actin-associating GIMAP4 is required for IFN-γ secretion during Th cell differentiation.Immunology and cell biology · 2015Article
- Variegated expression of Hsp22 transgenic reporters indicates cell-specific patterns of aging in Drosophila oenocytes.The journals of gerontology. Series A, Biological sciences and medical sciences · 2014Article
- Gimap and T cells: a matter of life or death.European journal of immunology · 2014Article
- Mitochondrial DNA genetics and the heteroplasmy conundrum in evolution and disease.Cold Spring Harbor perspectives in biology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial DNA (mtDNA) is a multi-copy genome encoding for proteins essential for aerobic energy metabolism. Mutations in mtDNA can lead to a variety of human diseases, from mild metabolic syndromes to severe fatal encephalomyopathies. Most mtDNA mutations co-exist with wild type genomes in a state known as heteroplasmy. The segregation of these pathogenic mutants is tissue and mutation specific, and a key determinant in the onset and severity of human mitochondrial disorders. We used a forward genetic approach in mice to identify and demonstrate that Gimap3 (GTP ase of immunity associated protein) is a key regulator of mtDNA segregation in leukocytes. The Gimap gene cluster is found only in vertebrates and appear to be a class of nucleotide-dependent dimerization GTP ases. Gimap3 is a membrane-anchored GTP ase with a critical role in T cell development. Here, we summarize our genetic findings and postulate how Gimap3 might regulate mtDNA genetics.
Identifiers
What OpenQuestion holds
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.