ArticlePloS one2013
Mitochondrial uptake of thiamin pyrophosphate: physiological and cell biological aspects.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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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
18 citing papers in PubMed, 28 citations in OpenAlex.
- Highly multiplexed mammalian metabolic engineering with a shotgun approach.Nature biotechnology · 2026Article
- Comparative Protective Effects of ATP and TPP Against Olaparib-Induced Ovarian Injury in Rats: Insights from Biochemical Parameters, Histopathology, and IRE1α, Cleaved Caspase-3, LC3B, and NF-κB p65 Double Immunofluorescence.Drug design, development and therapy · 2026Article
- Effect of IL-1β on pancreatic acinar cells mitochondrial TPP carrier-mediated uptake: inhibition mediated via the intracellular NF-κB signaling pathway.American journal of physiology. Cell physiology · 2025Article
- Intestinal Metabolome for Diagnosing and Prognosing Autism Spectrum Disorder in Children: A Systematic Review.Metabolites · 2025Review
- Effects of β-sitosterol on anxiety in migraine-induced rats: The role of oxidative/nitrosative stress and mitochondrial function.CNS neuroscience & therapeutics · 2024Article
- miR-122-5p is involved in posttranscriptional regulation of the mitochondrial thiamin pyrophosphate transporter (American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- The association of dietary intake of riboflavin and thiamine with kidney stone: a cross-sectional survey of NHANES 2007-2018.BMC public health · 2023Article
- Nutrients to Improve Mitochondrial Function to Reduce Brain Energy Deficit and Oxidative Stress in Migraine.Nutrients · 2021Review
- The coenzyme thiamine diphosphate displays a daily rhythm in the Arabidopsis nucleus.Communications biology · 2020Article
- Article
- Functional analysis of the third identified SLC25A19 mutation causative for the thiamine metabolism dysfunction syndrome 4.Journal of human genetics · 2019Article
- Engineering energetically efficient transport of dicarboxylic acids in yeastProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Adaptive regulation of pancreatic acinar mitochondrial thiamin pyrophosphate uptake process: possible involvement of epigenetic mechanism(s).American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Correction: Mitochondrial Uptake of Thiamin Pyrophosphate: Physiological and Cell Biological Aspects.PloS one · 2017Article
- Structure-function characterization of the human mitochondrial thiamin pyrophosphate transporter (hMTPPT; SLC25A19): Important roles for Ile(33), Ser(34), Asp(37), His(137) and Lys(291).Biochimica et biophysica acta · 2016Article
- Sexual Dimorphism and Aging in the Human Hyppocampus: Identification, Validation, and Impact of Differentially Expressed Genes by Factorial Microarray and Network Analysis.Frontiers in aging neuroscience · 2016Article
- Thiamine Deficiency in Tropical Pediatrics: New Insights into a Neglected but Vital Metabolic Challenge.Frontiers in nutrition · 2016Review
- Chronic alcohol exposure affects pancreatic acinar mitochondrial thiamin pyrophosphate uptake: studies with mouse 266-6 cell line and primary cells.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mammalian cells obtain vitamin B1 (thiamin) from their surrounding environment and convert it to thiamin pyrophosphate (TPP) in the cytoplasm. Most of TPP is then transported into the mitochondria via a carrier-mediated process that involves the mitochondrial thiamin pyrophosphate transporter (MTPPT). Knowledge about the physiological parameters of the MTPP-mediated uptake process, MTPPT targeting and the impact of clinical mutations in MTPPT in patients with Amish lethal microcephaly and neuropathy and bilateral striatal necrosis are not fully elucidated, and thus, were addressed in this study using custom-made (3)H-TPP as a substrate and mitochondria isolated from mouse liver and human-derived liver HepG2 cells. Results showed (3)H-TPP uptake by mouse liver mitochondria to be pH-independent, saturable (Km = 6.79±0.53 µM), and specific for TPP. MTPPT protein was expressed in mouse liver and HepG2 cells, and confocal images showed a human (h)MTPPT-GFP construct to be targeted to mitochondria of HepG2 cells. A serial truncation analysis revealed that all three modules of hMTPPT protein cooperated (although at different levels of efficiency) in mitochondrial targeting rather than acting autonomously as independent targeting module. Finally, the hMTPPT clinical mutants (G125S and G177A) showed proper mitochondrial targeting but displayed significant inhibition in (3)H-TPP uptake and a decrease in level of expression of the MTPPT protein. These findings advance our knowledge of the physiology and cell biology of the mitochondrial TPP uptake process. The results also show that clinical mutations in the hMTPPT system impair its functionality via affecting its level of expression with no effect on its targeting to mitochondria.
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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.