{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Akalu YT"],"funding":["Yale University","NEI NIH HHS","NCATS NIH HHS","NIDDK NIH HHS","Howard Hughes Medical Institute","Yale Cancer Center","National Cancer Institute","Dutch Cancer Society","NCI NIH HHS","National Institutes of Health","Fordham University","National Science Foundation"],"pagination":["e80530"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9433089"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11"],"pubmed_abstract":["Knockout (KO) mouse models play critical roles in elucidating biological processes behind disease-associated or disease-resistant traits. As a presumed consequence of gene KO, mice display certain phenotypes. Based on insight into the molecular role of said gene in a biological process, it is inferred that the particular biological process causally underlies the trait. This approach has been crucial towards understanding the basis of pathological and/or advantageous traits associated with <i>Mertk</i> KO mice. <i>Mertk</i> KO mice suffer from severe, early-onset retinal degeneration. MERTK, expressed in retinal pigment epithelia, is a receptor tyrosine kinase with a critical role in phagocytosis of apoptotic cells or cellular debris. Therefore, early-onset, severe retinal degeneration was "],"journal":["eLife"],"pubmed_title":["Tissue-specific modifier alleles determine <i>Mertk</i> loss-of-function traits."],"pmcid":["PMC9433089"],"funding_grant_id":["R01 EY026215","YSPORE Career Development Award DRP27","BUIT 2012-5347","2T32CA193200-06","DGE-1122492","Kim B. and Stephen E. Bepler Professorship in Biology","P30 DK034989","UL1 TR001863","Richard K. Gershon Fellowship","T32 CA193200","R01CA212376","R01 CA212376"],"pubmed_authors":["Nevin J","Finnemann SC","Lasorella A","Philbrick WM","Iavarone A","Ansems M","Alberto EJ","Alvarado D","Akalu YT","Ghosh S","Liu XN","He LZ","Mercau ME","Hughes LD","Bosenberg M","Rothlin CV","Keler T","Kong Y"],"additional_accession":[]},"is_claimable":false,"name":"Tissue-specific modifier alleles determine <i>Mertk</i> loss-of-function traits.","description":"Knockout (KO) mouse models play critical roles in elucidating biological processes behind disease-associated or disease-resistant traits. As a presumed consequence of gene KO, mice display certain phenotypes. Based on insight into the molecular role of said gene in a biological process, it is inferred that the particular biological process causally underlies the trait. This approach has been crucial towards understanding the basis of pathological and/or advantageous traits associated with <i>Mertk</i> KO mice. <i>Mertk</i> KO mice suffer from severe, early-onset retinal degeneration. MERTK, expressed in retinal pigment epithelia, is a receptor tyrosine kinase with a critical role in phagocytosis of apoptotic cells or cellular debris. Therefore, early-onset, severe retinal degeneration was ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-05-31T16:04:40.978Z","creation":"2025-02-19T01:27:01.286Z"},"accession":"S-EPMC9433089","cross_references":{"pubmed":["35969037"],"doi":["10.7554/eLife.80530"]}}