Ask about this productRelated genes to: PYCR1 Blocking Peptide
- Gene:
- PYCR1 NIH gene
- Name:
- pyrroline-5-carboxylate reductase 1
- Previous symbol:
- -
- Synonyms:
- P5C
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-24
- Date modifiied:
- 2015-09-07
Related products to: PYCR1 Blocking Peptide
Related articles to: PYCR1 Blocking Peptide
- Proline metabolism has been associated with schizophrenia pathophysiology; however, the underlying molecular mechanisms remain elusive. This study aimed to investigate the changes in the entire proline metabolic pathway in postmortem brains of patients with schizophrenia. Herein, enzyme-linked immunosorbent assay was performed to determine the protein levels of proline metabolism-associated key enzymes (prolidase [PEPD], proline dehydrogenase [PRODH], pyrroline-5-carboxylate synthetase [ALDH18A1], ornithine aminotransferase [OAT], and pyrroline-5-carboxylate reductase 1 [PYCR1]). Additionally, amino acids metabolized through the proline pathway, including proline, ornithine, and glutamic acid, were quantitatively analyzed through liquid chromatography-tandem mass spectrometry. The alterations in the expression of proline metabolism-associated enzymes and associated amino acid levels were analyzed in the postmortem brains of individuals with schizophrenia, and their associations with premortem clinical symptom scores were examined. Notably, in patients with schizophrenia, PRODH and PYCR1 expression significantly decreased in the superior temporal gyrus and prefrontal cortex, respectively, whereas amino acid levels showed no significant differences. Overall, the findings of this study show that dysregulation in proline metabolism may contribute to mitochondrial dysfunction owing to its close association with energy production and redox regulation. These results suggest the underlying pathophysiology of schizophrenia and provide insights for developing novel therapeutic strategies for managing schizophrenia. - Source: PubMed
Publication date: 2026/06/26
Nagaoka AtsukoHino MizukiShishido RisaHatano MasatakaHosogai YutoKano AkimuHamasaki HideomiKakita AkiyoshiTomita HiroakiKunii Yasuto - Microgravity during spaceflight is increasingly associated with cutaneous impairment, yet the structural basis and underlying metabolic mechanisms remain poorly defined. Collagen, the main component of the dermal extracellular matrix (ECM), relies on de novo proline synthesis in fibroblasts. Herein, we examined whether simulated microgravity (SMG) affects collagen synthesis by altering the proline biosynthetic pathway. - Source: PubMed
Publication date: 2026/06/25
Wang WenbinPeng XiufenLuo QingSong Guanbin - Pyrroline-5-carboxylate reductase 1 (PYCR1), a key enzyme in proline biosynthesis, has been implicated in various cancers. However, its role in clear cell renal cell carcinoma (ccRCC) remains elusive. - Source: PubMed
Publication date: 2026/06/23
Zhou JizheZhou YutingLi HaifengJiang MinlinGuo YueyueXie DelongYi SanguiLiu Zongling - Osteosarcoma treatment outcomes are compromised by increased drug resistance, distant metastasis, and tumor recurrence. While Pyrrolidine-5-carboxylic acid reductase 1(PYCR1) knockdown has been shown to inhibit tumor proliferation and migration in certain cancers. Its effects in osteosarcoma and regulatory mechanisms within osteosarcoma cells have not been explored. This study investigated the role of PYCR1 in osteosarcoma proliferation and its potential molecular mechanisms. The expression of PYCR1 was assessed in osteosarcoma tissues by immunohistochemistry and its correlation with clinical outcomes was determined. Subsequently, lentivirus-mediated knockdown and over expression of PYCR1 was achieved in osteosarcoma cells to evaluate its impact on proliferation, colony formation, and migration ability. The PI3K/Akt signaling pathway and its downstream effector COL1A1 were investigated using a combination of biomarker analysis, transcriptome sequencing, and co-immunoprecipitation assays. Subsequent silencing of COL1A1 induced phenotypic changes and confirmed tumorigenicity in vivo. The ferroptosis agonist Erastin and its specific antagonist Ferrostatin-1 (Fer-1) were combined with PYCR1 knockdown to explore their correlation with ferroptosis. By applying the pathway inhibitor LY294002, it was confirmed that the PI3K/Akt pathway is crucial for osteosarcoma proliferation. This study confirms that PYCR1 drives osteosarcoma cell proliferation and migration through three key mechanisms: regulating downstream genes, inhibiting ferroptosis, and activating the PI3K/Akt signaling pathway. - Source: PubMed
Publication date: 2026/06/19
Hu JianhuaHuang YiyuanChen HaomingXie ZehaoYan HanLi HaomiaoLi Runguang - Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Glutamine plays a critical role in the progression of LUAD. However, the function of pyrroline-5-carboxylate reductase 1 (PYCR1) and its regulatory role in glutamine metabolism remain unclear. Transcriptomic and clinical data for LUAD were obtained from The Cancer Genome Atlas (TCGA) and validated using Gene Expression Omnibus (GEO) datasets (GSE19188, GSE13213). Glutamine metabolism-related genes were analyzed for differential expression and prognostic significance. Functional enrichment was performed via gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analyses. Single-cell RNA-seq data (GSE117570) were processed using Seurat, and cell-cell communication was inferred with CellChat. In vitro, lentiviral overexpression, Western blotting, EdU, CCK-8, and glutamine uptake assays were conducted. An orthotopic xenograft model was established in nude mice to assess tumor growth in vivo. Six glutamine-metabolism-related genes were found significantly overexpressed in LUAD tissues and associated with poor overall survival. Single-cell sequencing revealed predominant PYCR1 expression in malignant cells. Functional assays demonstrated that PYCR1 overexpression enhanced glutamine uptake, proliferation, and inhibited apoptosis in LUAD cells, effects mediated via suppression of the P53 pathway. PYCR1 promoted tumor growth in a xenograft model and was found to transcriptionally upregulate 5-oxoprolinase (OPLAH), which augmented its oncogenic effects. Our findings identify the PYCR1/OPLAH axis as a key driver of LUAD progression via p53 signaling, revealing a promising therapeutic target. - Source: PubMed
Publication date: 2026/06/15
Chen WeiWang KaiWang RenyuDeng XufengLiu XiaobingDai PengLiu Quanxing