ArticlePloS one2015
DAPIT Over-Expression Modulates Glucose Metabolism and Cell Behaviour in HEK293T Cells.
Article in PloS one, 2015. 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 16 papers.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
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- A comprehensive transcriptomic analysis of the bisphenol A affected kidney in mice.Frontiers in molecular biosciences · 2023Article
- Integrative Analysis of Bulk RNA-Seq and Single-Cell RNA-Seq Unveils Novel Prognostic Biomarkers in Multiple Myeloma.Biomolecules · 2022Article
- Acetaldehyde Induces Cytotoxicity via Triggering Mitochondrial Dysfunction and Overactive Mitophagy.Molecular neurobiology · 2022Article
- The Ginsenoside RgLife (Basel, Switzerland) · 2021Article
- Whole‑genome identification and systematic analysis of lncRNA‑mRNA co‑expression profiles in patients with cutaneous basal cell carcinoma.Molecular medicine reports · 2021Article
- Article
- Mapping of cis-acting expression quantitative trait loci in human scalp hair follicles.BMC dermatology · 2020Article
- Weighted gene coexpression network analysis identifies hub genes related to KRAS mutant lung adenocarcinoma.Medicine · 2020Article
- Glucose-Induced Expression of DAPIT in Pancreatic β-Cells.Biomolecules · 2020Article
- Heat Failure Phenotypes Induced by Knockdown of DAPIT in Zebrafish: A New Insight into Mechanism of Dilated Cardiomyopathy.Scientific reports · 2017Article
- Deficiency in Kelch protein Klhl31 causes congenital myopathy in mice.The Journal of clinical investigation · 2017Article
- Regulation of the HCellular and molecular life sciences : CMLS · 2017Review
- Correction: DAPIT Over-Expression Modulates Glucose Metabolism and Cell Behaviour in HEK293T Cells.PloS one · 2015Article
- Correction: DAPIT Over-Expression Modulates Glucose Metabolism and Cell Behaviour in HEK293T Cells.PloS one · 2015Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionDiabetes Associated Protein in Insulin-sensitive Tissues (DAPIT) is a subunit of mitochondrial ATP synthase and has also been found to associate with the vacuolar H+-ATPase. Its expression is particularly high in cells with elevated aerobic metabolism and in epithelial cells that actively transport nutrients and ions. Deletion of DAPIT is known to induce loss of mitochondrial ATP synthase but the effects of its over-expression are obscure.
resultsIn order to study the consequences of high expression of DAPIT, we constructed a transgenic cell line that constitutively expressed DAPIT in human embryonal kidney cells, HEK293T. Enhanced DAPIT expression decreased mtDNA content and mitochondrial mass, and saturated respiratory chain by decreasing H+-ATP synthase activity. DAPIT over-expression also increased mitochondrial membrane potential and superoxide level, and translocated the transcription factors hypoxia inducible factor 1α (Hif1α) and β-catenin to the nucleus. Accordingly, cells over-expressing DAPIT used more glucose and generated a larger amount of lactate compared to control cells. Interestingly, these changes were associated with an epithelial to mesenchymal (EMT)-like transition by changing E-cadherin to N-cadherin and up-regulating several key junction/adhesion proteins. At physiological level, DAPIT over-expression slowed down cell growth by G1 arrest and migration, and enhanced cell detachment. Several cancers also showed an increase in genomic copy number of Usmg5 (gene encoding DAPIT), thereby providing strong correlative evidence for DAPIT possibly having oncogenic function in cancers.
conclusionsDAPIT over-expression thus appears to modulate mitochondrial functions and alter cellular regulations, promote anaerobic metabolism and induce EMT-like transition. We propose that DAPIT over-expression couples the changes in mitochondrial metabolism to physiological and pathophysiological regulations, and suggest it could play a critical role in H+-ATP synthase dysfunctions.
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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.