2004
DOI: 10.1128/mcb.24.2.527-536.2004
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Slc25a13-Knockout Mice Harbor Metabolic Deficits but Fail To Display Hallmarks of Adult-Onset Type II Citrullinemia

Abstract: Adult-onset type II citrullinemia (CTLN2) is an autosomal recessive disease caused by mutations in SLC25A13, the gene encoding the mitochondrial aspartate/glutamate carrier citrin. The absence of citrin leads to a liver-specific, quantitative decrease of argininosuccinate synthetase (ASS), causing hyperammonemia and citrullinemia. To investigate the physiological role of citrin and the development of CTLN2, an Slc25a13-knockout (also known as Ctrn-deficient) mouse model was created. The resulting Ctrn ؊/؊ mice… Show more

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Cited by 70 publications
(79 citation statements)
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“…1). Comparisons between wild-type and Ctrn-KO mice also showed similar growth rates (42), and mGPD-KO mice showed only a small difference in growth rate compared with non-littermate wild-type mice (data not shown).…”
Section: Decreased Survival and Growth Retardation Of Ctrn/mgpdmentioning
confidence: 76%
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“…1). Comparisons between wild-type and Ctrn-KO mice also showed similar growth rates (42), and mGPD-KO mice showed only a small difference in growth rate compared with non-littermate wild-type mice (data not shown).…”
Section: Decreased Survival and Growth Retardation Of Ctrn/mgpdmentioning
confidence: 76%
“…Animals-Mice homozygous for the targeted disruption of the Slc25a13 gene that encodes citrin (Ctrn Ϫ/Ϫ or Ctrn-KO) and for the mGPD gene that encodes mGPD (mGPD Ϫ/Ϫ or mGPD-KO) were generated as described previously (42,45). Both KO mutations were made congenic on the C57BL/6J genetic background by backcrossing for at least nine generations.…”
Section: Methodsmentioning
confidence: 99%
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