<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dubail J</submitter><funding>NICHD NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>National Institutes of Health</funding><funding>KNIGHTS TEMPLAR EYE FOUNDATION</funding><pagination>702-12</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4107014</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>52(7)</volume><pubmed_abstract>ADAMTS9 is the most conserved member of a large family of secreted metalloproteases having diverse functions. Adamts9 null mice die before gastrulation, precluding investigations of its roles later in embryogenesis, in adult mice or disease models. We therefore generated a floxed Adamts9 allele to bypass embryonic lethality. In this mutant, unidirectional loxP sites flank exons 5-8, which encode the catalytic domain, including the protease active site. Mice homozygous for the floxed allele were viable, lacked an overt phenotype, and were fertile. Conversely, mice homozygous for a germ-line deletion produced from the floxed allele by Cre-lox recombination did not survive past gastrulation. Hemizygosity of the deleted Adamts9 in combination with mutant Adamts20 led to cleft palate and severe</pubmed_abstract><journal>Genesis (New York, N.Y. : 2000)</journal><pubmed_title>A new Adamts9 conditional mouse allele identifies its non-redundant role in interdigital web regression.</pubmed_title><pmcid>PMC4107014</pmcid><funding_grant_id>T32 HL007914</funding_grant_id><funding_grant_id>P01 HL107147</funding_grant_id><funding_grant_id>HL107147</funding_grant_id><funding_grant_id>HD069747</funding_grant_id><funding_grant_id>HL007914</funding_grant_id><funding_grant_id>T32HL007914-08</funding_grant_id><funding_grant_id>R01 HD069747</funding_grant_id><funding_grant_id>-</funding_grant_id><funding_grant_id>R03 HD069747</funding_grant_id><pubmed_authors>Bader HL</pubmed_authors><pubmed_authors>Nelson CM</pubmed_authors><pubmed_authors>Dubail J</pubmed_authors><pubmed_authors>Matuska B</pubmed_authors><pubmed_authors>Apte SS</pubmed_authors><pubmed_authors>Katebi N</pubmed_authors><pubmed_authors>Aramaki-Hattori N</pubmed_authors><pubmed_authors>Olsen BR</pubmed_authors></additional><is_claimable>false</is_claimable><name>A new Adamts9 conditional mouse allele identifies its non-redundant role in interdigital web regression.</name><description>ADAMTS9 is the most conserved member of a large family of secreted metalloproteases having diverse functions. Adamts9 null mice die before gastrulation, precluding investigations of its roles later in embryogenesis, in adult mice or disease models. We therefore generated a floxed Adamts9 allele to bypass embryonic lethality. In this mutant, unidirectional loxP sites flank exons 5-8, which encode the catalytic domain, including the protease active site. Mice homozygous for the floxed allele were viable, lacked an overt phenotype, and were fertile. Conversely, mice homozygous for a germ-line deletion produced from the floxed allele by Cre-lox recombination did not survive past gastrulation. Hemizygosity of the deleted Adamts9 in combination with mutant Adamts20 led to cleft palate and severe</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jul</publication><modification>2025-05-29T22:09:32.533Z</modification><creation>2019-03-27T01:32:34Z</creation></dates><accession>S-EPMC4107014</accession><cross_references><pubmed>24753090</pubmed><doi>10.1002/dvg.22784</doi></cross_references></HashMap>