ArticlePloS one2013
Kinetic and structural evidences on human prolidase pathological mutants suggest strategies for enzyme functional rescue.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Validated analytical workflow for quantifying proline metabolism related amino acids in HaCaT cells with LC-Q-TOF-MS.Scientific reports · 2026Article
- Novel epigenetic marks of insulin resistance trajectories in a longitudinal study of childhood obesity.Cardiovascular diabetology · 2026Article
- Interstitial Lung Disease in a Girl with Prolidase Deficiency.Journal of clinical immunology · 2025Article
- Consequences of Disturbing Manganese Homeostasis.International journal of molecular sciences · 2023Review
- Recombinant Human Prolidase (rhPEPD) Induces Wound Healing in Experimental Model of Inflammation through Activation of EGFR Signalling in Fibroblasts.Molecules (Basel, Switzerland) · 2023Article
- Article
- Recombinant Prolidase Activates EGFR-Dependent Cell Growth in an Experimental Model of Inflammation in HaCaT Keratinocytes. Implication for Wound Healing.Frontiers in molecular biosciences · 2022Article
- Structural analysis of new compound heterozygous variants in PEPD gene identified in a patient with Prolidase Deficiency diagnosed by exome sequencing.Genetics and molecular biology · 2021Article
- Review
- Comprehensive in-silico prediction of damage associated SNPs in Human Prolidase gene.Scientific reports · 2018Article
- PEPD is a pivotal regulator of p53 tumor suppressor.Nature communications · 2017Article
- Article
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12 authors.
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Abstract
Prolidase is the only human enzyme responsible for the digestion of iminodipeptides containing proline or hydroxyproline at their C-terminal end, being a key player in extracellular matrix remodeling. Prolidase deficiency (PD) is an intractable loss of function disease, characterized by mutations in the prolidase gene. The exact causes of activity impairment in mutant prolidase are still unknown. We generated three recombinant prolidase forms, hRecProl-231delY, hRecProl-E412K and hRecProl-G448R, reproducing three mutations identified in homozygous PD patients. The enzymes showed very low catalytic efficiency, thermal instability and changes in protein conformation. No variation of Mn(II) cofactor affinity was detected for hRecProl-E412K; a compromised ability to bind the cofactor was found in hRecProl-231delY and Mn(II) was totally absent in hRecProl-G448R. Furthermore, local structure perturbations for all three mutants were predicted by in silico analysis. Our biochemical investigation of the three causative alleles identified in perturbed folding/instability, and in consequent partial prolidase degradation, the main reasons for enzyme inactivity. Based on the above considerations we were able to rescue part of the prolidase activity in patients' fibroblasts through the induction of Heath Shock Proteins expression, hinting at new promising avenues for PD treatment.
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