ArticleMolecular genetics and metabolism2015
Gene expression in cell lines from propionic acidemia patients, carrier parents, and controls.
Article in Molecular genetics and metabolism, 2015. 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, 8 citations in OpenAlex.
- Precision metabolic therapy for propionic acidemia.Biochemical pharmacology · 2026Review
- Elevated propionate and its association with neurological dysfunctions in propionic acidemia.Frontiers in molecular neuroscience · 2025Review
- Pathophysiological mechanisms of complications associated with propionic acidemia.Pharmacology & therapeutics · 2023Review
- The anti-inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters.Food science & nutrition · 2021Article
- Biochemical and anaplerotic applications of in vitro models of propionic acidemia and methylmalonic acidemia using patient-derived primary hepatocytes.Molecular genetics and metabolism · 2020Article
- Recapitulation of metabolic defects in a model of propionic acidemia using patient-derived primary hepatocytes.Molecular genetics and metabolism · 2016Article
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 1 country.
Funding
Abstract
Propionic acidemia (PA) is an inborn of metabolism which usually presents with metabolic acidosis and accumulation of 3-hydroxypropionate among other toxins. Examining the gene expression in lymphoblastoid cell lines (LCLs) from PA patients, their carrier parents and age/sex-matched controls at normal glucose and low glucose growth conditions demonstrated differences among and between these groups. Using three-way ANOVA analysis, four DAVID clusters of response were identified of which three of the four clusters showed that LCLs from carrier parents had an intermediate response between healthy controls and PA patients. These differences included changes in expression of cell cycle regulatory genes, mitochondrial related genes, and transcriptional regulation. In addition, differences also were observed in expression of genes involved in transendothelial migration and focal adhesion at normal growth conditions when comparing the LCLs from PA patients and controls. These studies demonstrate transcriptional differences between LCLs from PA patients, their parents and biochemically normal controls.
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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.