PSRC1

Last update 08 May 2025

Basic Info

Synonyms

DDA3, proline and serine rich coiled-coil 1, Proline/serine-rich coiled-coil protein 1

+ [1]

Introduction

Required for normal progression through mitosis. Required for normal congress of chromosomes at the metaphase plate, and for normal rate of chromosomal segregation during anaphase. Plays a role in the regulation of mitotic spindle dynamics. Increases the rate of turnover of microtubules on metaphase spindles, and contributes to the generation of normal tension across sister kinetochores. Recruits KIF2A and ANKRD53 to the mitotic spindle and spindle poles. May participate in p53/TP53-regulated growth suppression.

100 Clinical Results associated with PSRC1

100 Translational Medicine associated with PSRC1

0 Patents (Medical) associated with PSRC1

127

Literatures (Medical) associated with PSRC1

01 Jul 2025·Biochemical Pharmacology

Phosphocreatine alleviates monocrotaline-induced liver injury dependent on PSRC1-regulated endoplasmic reticulum stress

Article

Author: Chen, Sinuo ; Ji, Mingyan ; Xia, Jinglin ; Jiang, Hongyue ; Gao, Hong ; Chen, Yun ; Li, Dongping ; Song, Guangqi ; Ma, Yifan ; Wang, Heming

Monocrotaline (MCT), a pyrrolizidine alkaloid (PA), is naturally found in certain plants and known for its hepatotoxic effects. In our prior research, we identified that phosphocreatine (PCr) mitigates PA-induced liver damage. However, the specific mechanism of PCr remains unknown. The objective of the present study was to elucidate the mechanism through which PCr shields against MCT-induced hepatic injury. In vitro assays demonstrated that PCr mitigated the MCT-induced ER stress and apoptosis. This alleviation was similarly observed with the use of the ER stress inhibitor 4-PBA, hinting at the role of ER stress in the protective mechanism of PCr against MCT-induced hepatic damage. In the MCT group, an upregulation of proline/serine-rich coiled-coil protein 1 (PSRC1) was evident, but this was notably downregulated following PCr treatment in vitro. The silencing of PSRC1 diminished the ER stress and apoptosis triggered by MCT, and the protective effect of PCr on liver injury remained evident. Overexpressing PSRC1 increased MCT-induced apoptosis and ER stress, and PCr still plays a protective role. In vivo experiments, we observed a notable attenuation of MCT-induced liver damage by PCr. Employing RNA sequencing and immunohistochemical staining techniques, we ascertained that endoplasmic reticulum (ER) stress, apoptosis and PSRC1 were significantly elevated in the liver samples treated with MCT. Notably, these alterations were counteracted by the presence of PCr. In conclusion, our findings suggest that PCr counteracts ER stress via modulation of PSRC1, which consequently confers protection against MCT-induced liver injury. Furthermore, this study offers potential therapeutic avenues for addressing hepatic damages attributable to MCT.

01 Apr 2025·Advanced Science

(Apo)Lipoprotein Profiling with Multi‐Omics Analysis Identified Medium‐HDL‐Targeting PSRC1 with Therapeutic Potential for Coronary Artery Disease

Article

Author: Liu, Ling ; Wang, Sihan ; Cai, Hao ; Li, Yingmei ; Wu, Qingqing ; Huang, Yacan ; Gao, Mingjing ; Zhang, Xiaogang ; Qiu, Gaokun

AbstractIdentification of (apo)lipoprotein subclasses causally underpinning atherosclerosis may lead to identification of novel drug targets for treatment of atherosclerotic cardiovascular disease (ASCVD). In this study, observational and genetic associations between (apo)lipoprotein profile and carotid intima‐media thickness‐assessed atherosclerosis, and risks of coronary artery disease (CAD) and ischemic stroke (IS) are assessed, using data from the UK Biobank study, with further exploration of potential drug target for these two ASCVD subtypes through multi‐omics analysis integrating genetic, transcriptomic, and proteomic data. Cholesteryl ester content in medium high‐density lipoprotein causally protective of atherosclerosis is identified, plus a target gene, PSRC1, with therapeutic potential for CAD, but not IS, supported by consistent evidence from multi‐omics layers of data, which also reveals that such therapeutic potential may be through downregulation of circulating proteins including TRP1, GRNs, and Pla2g12b, and upregulation of Neo1. The results provide strong evidence as well as mechanistic clues of PSRC1’s therapeutic potential for CAD.

01 Mar 2025·Gene

VAMP8 as a biomarker and potential therapeutic target for endothelial cell dysfunction in atherosclerosis

Article

Author: Yang, Luqun ; Shi, Xiushan ; Yao, Huijing ; Zhu, Kaiyi ; Li, Bingjie ; Gao, Yuping ; Guan, Xin ; Lin, Yuanyuan ; Cheng, Jiangwei ; Ni, Lin

BACKGROUNDEndothelial cell dysfunction has a critical role in the pathophysiology of atherosclerosis. This study aims to uncover pivotal genes and pathways linked to endothelial cell dysfunction in atherosclerosis, as well as to ascertain the assumed causal effects and potential mechanisms.METHODSDatasets relevant to endothelial cell dysfunction in atherosclerosis were collected and divided into training and validation sets. Following differential analysis, we constructed a protein-protein interaction (PPI) network and a molecular interaction map of common-differentially expressed genes (co-DEGs) with proteins known to be involved in atherosclerotic endothelial cell dysfunction. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genome (KEGG), and Gene Set Enrichment Analysis (GSEA) were also conducted. Moreover, human umbilical vein endothelial cells (HUVECs) were cultured in circumstances characterized by elevated glucose levels to establish a cellular injury model simulating atherosclerotic conditions, and quantitative Polymerase Chain Reaction (qPCR) experiments were conducted to validate the differences of co-DEGs. Subsequently, the Summary-data-based Mendelian Randomization (SMR) method was employed. Additionally, we employed the Western Blot (WB) technique to validate the differential expression of VAMP8. Finally, we identified the differential expression of VAMP8 in the validation set and further validated its differential expression by collecting fresh blood samples from 20 patients with atherosclerosis and 20 healthy individuals.RESULTS14 co-DEGs (FABP5, GULP1, COL4A5, VAMP8, FABP4, PFN2, ANGPT2, TFPI2, NUPR1, SULF1, FGF13, BASP1, EPB41L3, and PBK) were identified. SMR analysis confirmed 10 potential causal effect genes: PSRC1, VAMP8, FES, HNRNPUL1, CFDP1, SAP130, MDN1, OPRL1, UTP11, and HOXC4. The qPCR and WB experiments demonstrated that VAMP8 was significantly upregulated in the injured HUVECs group (p < 0.0001). Compared to the control group, VAMP8 was markedly increased in the blood samples of patients with atherosclerosis (p < 0.0001).CONCLUSIONSVAMP8 may potentially serve as a pathogenic gene in the process of endothelial dysfunction in atherosclerosis.

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PSRC1

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