<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Akalu YT</submitter><funding>Yale University</funding><funding>NEI NIH HHS</funding><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>Howard Hughes Medical Institute</funding><funding>Yale Cancer Center</funding><funding>National Cancer Institute</funding><funding>Dutch Cancer Society</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>Fordham University</funding><funding>National Science Foundation</funding><pagination>e80530</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9433089</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11</volume><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 &lt;i>Mertk&lt;/i> KO mice. &lt;i>Mertk&lt;/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 </pubmed_abstract><journal>eLife</journal><pubmed_title>Tissue-specific modifier alleles determine &lt;i>Mertk&lt;/i> loss-of-function traits.</pubmed_title><pmcid>PMC9433089</pmcid><funding_grant_id>R01 EY026215</funding_grant_id><funding_grant_id>YSPORE Career Development Award DRP27</funding_grant_id><funding_grant_id>BUIT 2012-5347</funding_grant_id><funding_grant_id>2T32CA193200-06</funding_grant_id><funding_grant_id>DGE-1122492</funding_grant_id><funding_grant_id>Kim B. and Stephen E. Bepler Professorship in Biology</funding_grant_id><funding_grant_id>P30 DK034989</funding_grant_id><funding_grant_id>UL1 TR001863</funding_grant_id><funding_grant_id>Richard K. Gershon Fellowship</funding_grant_id><funding_grant_id>T32 CA193200</funding_grant_id><funding_grant_id>R01CA212376</funding_grant_id><funding_grant_id>R01 CA212376</funding_grant_id><pubmed_authors>Nevin J</pubmed_authors><pubmed_authors>Finnemann SC</pubmed_authors><pubmed_authors>Lasorella A</pubmed_authors><pubmed_authors>Philbrick WM</pubmed_authors><pubmed_authors>Iavarone A</pubmed_authors><pubmed_authors>Ansems M</pubmed_authors><pubmed_authors>Alberto EJ</pubmed_authors><pubmed_authors>Alvarado D</pubmed_authors><pubmed_authors>Akalu YT</pubmed_authors><pubmed_authors>Ghosh S</pubmed_authors><pubmed_authors>Liu XN</pubmed_authors><pubmed_authors>He LZ</pubmed_authors><pubmed_authors>Mercau ME</pubmed_authors><pubmed_authors>Hughes LD</pubmed_authors><pubmed_authors>Bosenberg M</pubmed_authors><pubmed_authors>Rothlin CV</pubmed_authors><pubmed_authors>Keler T</pubmed_authors><pubmed_authors>Kong Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tissue-specific modifier alleles determine &lt;i>Mertk&lt;/i> loss-of-function traits.</name><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 &lt;i>Mertk&lt;/i> KO mice. &lt;i>Mertk&lt;/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 </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Aug</publication><modification>2026-05-31T16:04:40.978Z</modification><creation>2025-02-19T01:27:01.286Z</creation></dates><accession>S-EPMC9433089</accession><cross_references><pubmed>35969037</pubmed><doi>10.7554/eLife.80530</doi></cross_references></HashMap>