Ask about this productRelated genes to: PCOLCE antibody
- Gene:
- PCOLCE NIH gene
- Name:
- procollagen C-endopeptidase enhancer
- Previous symbol:
- -
- Synonyms:
- PCPE, PCPE1
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-17
- Date modifiied:
- 2016-10-05
Related products to: PCOLCE antibody
Related articles to: PCOLCE antibody
- Women often experience greater disability after ischemic stroke than men, but the biological mechanisms underlying these differences remain unclear. Proteomic analysis may identify sex-specific molecular pathways that contribute to stroke rehabilitation and recovery. - Source: PubMed
Publication date: 2026/04/19
McLouth Christopher JHazelwood Hunter SFrank Jacqueline AHarp Jordan PDornbos DavidFraser Justin FPennypacker Keith R - The extracellular matrix (ECM) plays a critical role in tumor progression by modulating cell adhesion, migration, and signaling; however, its contribution to metastatic progression in spontaneous mammary tumors remains poorly understood. Mammary tumors are among the most common neoplasms in female dogs and share histopathological and molecular similarities with human breast cancer, supporting their use as a comparative oncology model. To investigate ECM remodeling during tumor progression, we analyzed normal, non-metastatic, and metastatic canine mammary tissues using histological approaches and label-free quantitative proteomics. Publicly available human breast cancer transcriptomic datasets were interrogated for validation of conserved molecular signatures. Proteomic profiling identified 12 differentially expressed ECM-related proteins: eight were upregulated (COL12A1, COL4A1, COL4A2, SERPINH1, SERPINF1, HTRA1, TNC, PCOLCE) and four were downregulated (MMRN1, ABI3BP, DPT, OGN). The downregulated proteins were further validated in human breast cancer transcriptomes. Collectively, these findings indicate active ECM remodeling during tumor progression, characterized by increased expression of proteins associated with matrix stiffness and invasiveness. This study highlights evolutionarily conserved mechanisms of ECM dysregulation in breast cancer and identifies potential matrix targets for translational research and biomarker development. - Source: PubMed
Publication date: 2026/03/24
de Almeida Bruno SousaRocha Gisele VieiraNunes SimoneZanette Dalila LuciolaBatista MichelEstrela-Lima AlessandraRegis-Silva Carlos GustavoDamasceno Karine Araújo - Asymptomatic Alzheimer's Disease (AsymAD) is a preclinical stage of Alzheimer's Disease (AD) identified by amyloid plaques and neurofibrillary tangles in cognitively normal individuals and offers essential understanding for early diagnosis and treatment of AD. To uncover molecular insights into AsymAD, RNA sequencing (RNA-seq) datasets from two different consortia, ROSMAP (Religious Orders Study and Memory and Aging Project) and MSBB (Mount Sinai Brain Bank), were investigated. The individuals in the datasets were grouped into AD and AsymAD based on clinical and neuropathological criteria. Differentially expressed genes (DEGs), differentially expressed transcripts (DETs), and differentially used transcripts (DUTs) were identified between AD and AsymAD samples. The results were interpreted through functional enrichment analysis and compared with the predefined lists of AD-related and learning-memory-cognition-related genes, and genes from an independent mouse dataset. The genes from the list of DEGs, DETs and DUTs were mapped onto a human protein-protein interaction network, revealing subnetworks associated with AsymAD. This led to the discovery of biomarker candidate genes: NRXN3, DGKB, ADAMTS2, GNG4, ENPP5, PCOLCE, COL25A1, COL26A1, MRPL1, and MRPL30. This study introduces an innovative approach by including DETs and DUTs in the analyses, beyond the standard focus on DEGs, pointing out comprehensive insights into the molecular mechanisms of AsymAD. In addition, combining the results of the subnetwork analysis from DEGs, DETs, and DUTs provided a new perspective to AsymAD and resulted in the discovery of further important genes, which can pave the way for early detection and intervention of AD. - Source: PubMed
Publication date: 2026/02/22
Aksu RümeysaLüleci Hatice BüşraÇakır Tunahan - PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibition is a potent cholesterol-lowering strategy. This study examined the effects of PCSK9 monoclonal antibodies (mAbs) and high-intensity statins beyond low-density lipoprotein cholesterol reduction, which are not fully defined, particularly in patients with acute myocardial infarction (MI). - Source: PubMed
Publication date: 2026/02/10
Schmidt Lukas EBurnap Sean ASingh BhawanaTakov KaloyanLosdat SylvainSchrutka LoreGalli LukasTheofilatos KonstantinosOtto Georg WHengstenberg ChristianTzoulaki IoannaLang Irene MKoskinas Konstantinos CSpeidl Walter SRäber LorenzMayr Manuel - Myopia, particularly pathological myopia (PM), poses a significant global health burden due to its increasing prevalence and associated vision-threatening complications. Despite extensive genetic research, the molecular mechanisms underlying myopia progression remain unclear. This study aims to identify key causal proteins and metabolic pathways in myopia and PM and explore potential therapeutic targets. - Source: PubMed
Publication date: 2026/01/08
Hui JingwenCui XuehaoHan Quanhong