{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Reventun P"],"funding":["NHLBI NIH HHS"],"pagination":["e323000"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12823045"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["46(3)"],"pubmed_abstract":["<h4>Background</h4>Abnormal levels of VWF (von Willebrand Factor) are a risk factor for venous thromboembolism (VTE) and bleeding. Genome-wide association studies for VWF have identified novel candidate genes that may regulate VWF levels in humans, including <i>RAB5C</i> (RAS [rat sarcoma]-associated protein RAB5C). We hypothesized that RAB5C regulates VWF release from endothelial cells.<h4>Methods</h4>We studied the effect of RAB5C on vesicle trafficking in human endothelial cells. We performed CRISPR (clustered regularly interspaced short palindromic repeats) interference targeting 2 genetic variants linked to altered VWF levels and evaluated RAB5C expression by reverse transcription-quantitative polymerase chain reaction. We silenced RAB5C or overexpressed RAB5C wild-type, constitutive "],"journal":["Arteriosclerosis, thrombosis, and vascular biology"],"pubmed_title":["RAB5C Increases Endothelial Release of VWF by Regulating Vesicle Trafficking."],"pmcid":["PMC12823045"],"funding_grant_id":["K08 HL166690","R01 HL173974","R01 HL164478","R33 HL141791","R01 HL139553","R61 HL141791","R01 HL126974","R01 HL174778","R01 HL105756"],"pubmed_authors":["Alcharani N","Reventun P","Arvanitis M","Gonzalez-Cucharero C","Sabater-Lleal M","Delgado-Marin M","Morrison AC","Osburn WO","Lowenstein CJ","Smith NL","Wolberg AS","Viskadourou M","Toledano-Sanz P","Cohorts for Heart and Aging in Genomic Epidemiology Hemostasis Working Group","Foster DB","de Vries PS"],"additional_accession":[]},"is_claimable":false,"name":"RAB5C Increases Endothelial Release of VWF by Regulating Vesicle Trafficking.","description":"<h4>Background</h4>Abnormal levels of VWF (von Willebrand Factor) are a risk factor for venous thromboembolism (VTE) and bleeding. Genome-wide association studies for VWF have identified novel candidate genes that may regulate VWF levels in humans, including <i>RAB5C</i> (RAS [rat sarcoma]-associated protein RAB5C). We hypothesized that RAB5C regulates VWF release from endothelial cells.<h4>Methods</h4>We studied the effect of RAB5C on vesicle trafficking in human endothelial cells. We performed CRISPR (clustered regularly interspaced short palindromic repeats) interference targeting 2 genetic variants linked to altered VWF levels and evaluated RAB5C expression by reverse transcription-quantitative polymerase chain reaction. We silenced RAB5C or overexpressed RAB5C wild-type, constitutive ","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Mar","modification":"2026-07-16T21:26:55.616Z","creation":"2026-07-10T03:14:57.288Z"},"accession":"S-EPMC12823045","cross_references":{"pubmed":["41537263"],"doi":["10.1161/atvbaha.125.323000","10.1161/ATVBAHA.125.323000"]}}