ArticleMolecular genetics and metabolism reports2023
Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver.
Article in Molecular genetics and metabolism reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 6 citations in OpenAlex.
- A transport-independent role for SLC25A12 in mitochondrial stress signalling.Nature cell biology · 2026Article
- Aspartate-Glutamate Carrier 1 (International journal of molecular sciences · 2026Review
- From the cytosol to the inner membrane: biogenesis of the mitochondrial carrier family.Protein science : a publication of the Protein Society · 2026Review
- Glycerol-3-phosphate activates ChREBP, FGF21 transcription and lipogenesis in citrin deficiency.Nature metabolism · 2025Article
- Mir-509-3p targets SLC25A13 to regulate ferroptosis and protect retinal endothelial cells in diabetic retinopathy.Acta diabetologica · 2025Article
- Current Understanding of Pathogenic Mechanisms and Disease Models of Citrin Deficiency.Journal of inherited metabolic disease · 2025Review
- My path to citrin deficiency.Journal of inherited metabolic disease · 2025Review
- The therapeutic landscape of citrin deficiency.Journal of inherited metabolic disease · 2024Review
- Calcium signaling in mitochondrial intermembrane space.Biochemical Society transactions · 2024Review
Corrections and comments
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Authors and funding
14 authors at 11 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The deficiency of CITRIN, the liver mitochondrial aspartate-glutamate carrier (AGC), is the cause of four human clinical phenotypes, neonatal intrahepatic cholestasis caused by CITRIN deficiency (NICCD), silent period, failure to thrive and dyslipidemia caused by CITRIN deficiency (FTTDCD), and citrullinemia type II (CTLN2). Clinical symptoms can be traced back to disruption of the malate-aspartate shuttle due to the lack of citrin. A potential therapy for this condition is the expression of aralar, the AGC present in brain, to replace citrin. To explore this possibility we have first verified that the NADH/NAD
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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.