<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>288(21)</volume><submitter>Lee GS</submitter><funding>Intramural NIH HHS</funding><pubmed_abstract>TTLL5/STAMP (tubulin tyrosine ligase-like family member 5) has multiple activities in cells. TTLL5 is one of 13 TTLLs, has polyglutamylation activity, augments the activity of p160 coactivators (SRC-1 and TIF2) in glucocorticoid receptor-regulated gene induction and repression, and displays steroid-independent growth activity with several cell types. To examine TTLL5/STAMP functions in whole animals, mice were prepared with an internal deletion that eliminated several activities of the Stamp gene. This mutation causes both reduced levels of STAMP mRNA and C-terminal truncation of STAMP protein. Homozygous targeted mutant (Stamp(tm/tm)) mice appear normal except for marked decreases in male fertility associated with defects in progressive sperm motility. Abnormal axonemal structures with lo</pubmed_abstract><journal>The Journal of biological chemistry</journal><pagination>15167-80</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3663537</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Disruption of Ttll5/stamp gene (tubulin tyrosine ligase-like protein 5/SRC-1 and TIF2-associated modulatory protein gene) in male mice causes sperm malformation and infertility.</pubmed_title><pmcid>PMC3663537</pmcid><pubmed_authors>Armstrong SP</pubmed_authors><pubmed_authors>Lee GS</pubmed_authors><pubmed_authors>Dougherty EJ</pubmed_authors><pubmed_authors>London EC</pubmed_authors><pubmed_authors>He Y</pubmed_authors><pubmed_authors>Jimenez-Movilla M</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Avella M</pubmed_authors><pubmed_authors>Grullon S</pubmed_authors><pubmed_authors>Blackford JA</pubmed_authors><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Awasthi S</pubmed_authors><pubmed_authors>Guo C</pubmed_authors><pubmed_authors>Simons SS</pubmed_authors><pubmed_authors>Sharlin DS</pubmed_authors><pubmed_authors>Dean J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Disruption of Ttll5/stamp gene (tubulin tyrosine ligase-like protein 5/SRC-1 and TIF2-associated modulatory protein gene) in male mice causes sperm malformation and infertility.</name><description>TTLL5/STAMP (tubulin tyrosine ligase-like family member 5) has multiple activities in cells. TTLL5 is one of 13 TTLLs, has polyglutamylation activity, augments the activity of p160 coactivators (SRC-1 and TIF2) in glucocorticoid receptor-regulated gene induction and repression, and displays steroid-independent growth activity with several cell types. To examine TTLL5/STAMP functions in whole animals, mice were prepared with an internal deletion that eliminated several activities of the Stamp gene. This mutation causes both reduced levels of STAMP mRNA and C-terminal truncation of STAMP protein. Homozygous targeted mutant (Stamp(tm/tm)) mice appear normal except for marked decreases in male fertility associated with defects in progressive sperm motility. Abnormal axonemal structures with lo</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 May</publication><modification>2026-04-13T13:54:07.857Z</modification><creation>2019-03-27T01:10:23Z</creation></dates><accession>S-EPMC3663537</accession><cross_references><pubmed>23558686</pubmed><doi>10.1074/jbc.M113.453936</doi><doi>10.1074/jbc.m113.453936</doi></cross_references></HashMap>