ArticleAmerican journal of human genetics1993
Cloning of functional alpha propionyl CoA carboxylase and correction of enzyme deficiency in pccA fibroblasts.
Article in American journal of human genetics, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 29 citations in OpenAlex.
- Celecoxib suppresses colorectal cancer growth by inhibiting propionyl-CoA carboxylase alpha chain-mediated epithelial-mesenchymal transition and angiogenesis.Gastroenterology report · 2026Article
- Silencing PCCA Suppresses CRC Growth and Spread by Modulating EMT and M1 Macrophage Polarization.International journal of medical sciences · 2025Article
- Multi-omics analysis identifies drivers of protein phosphorylation.Genome biology · 2023Article
- Genome-Wide Association Study Identifies Genomic Loci Associated With Neurotransmitter Concentration in Cattle.Frontiers in genetics · 2020Article
- Spectrum of mutations underlying Propionic acidemia and further insight into a genotype-phenotype correlation for the common mutation in Saudi Arabia.Molecular genetics and metabolism reports · 2019Article
- Adenovirus-mediated gene delivery rescues a neonatal lethal murine model of mut(0) methylmalonic acidemia.Human gene therapy · 2008Article
- Human propionyl-CoA carboxylase beta subunit gene: exon-intron definition and mutation spectrum in Spanish and Latin American propionic acidemia patients.American journal of human genetics · 1998Article
- Clinical outcome and long-term management of 17 patients with propionic acidaemia.European journal of pediatrics · 1996Article
- Mutations participating in interallelic complementation in propionic acidemia.American journal of human genetics · 1994Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Propionyl CoA carboxylase (PPC) is a heteromeric enzyme composed of alpha subunits (PCCA) and beta (PCCB) subunits. We describe cDNA clones expressing human PCCA and complementation of the genetic defect in pccA fibroblasts by DNA-mediated gene transfer. Two cDNA clones were constructed. The first corresponds to the previously reported, putatively full-length, open reading frame. The second encodes a chimera composed of the mitochondrial leader sequence of human methylmalonyl CoA mutase and the mature PCCA protein. Both clones reconstitute propionate flux to normal levels in fibroblasts from patients genetically deficient in PCCA (pccA). The maximal level of propionate flux approached, but never exceeded, the levels seen in control plates of normal cells. In contrast, the maximal level of PPC holoenzyme activity reached only 10%-20% that of normal controls, which corresponded roughly to the fraction of cells actually transformed with the recombinant gene. These data suggest that the level of PCCA expression in fibroblasts does not normally limit PCC holoenzyme activity or propionate flux. The fact that a small fraction of cells reconstitutes propionate flux to normal levels suggests that metabolic cooperation between cells is capable of increasing the metabolic capacity of recombinant enzyme in a subpopulation of cells. These factors may have important implications for the rational design of somatic gene therapy for PCCA deficiency.
Indexed as
Identifiers
8434582PMC1682099W1469706263What OpenQuestion holds
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.