<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pires ES</submitter><funding>NICHD NIH HHS</funding><funding>NCATS NIH HHS</funding><funding>FIC NIH HHS</funding><funding>NIH HHS</funding><pagination>1405-26</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4091973</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>242(12)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Sperm Acrosomal SLLP1 Binding (SAS1B) protein (ovastacin) is an oolemmal binding partner for the intra-acrosomal sperm protein SLLP1.&lt;h4>Results&lt;/h4>Immunohistochemical localization revealed that SAS1B translation is restricted among adult tissues to the ovary and oocytes, SAS1B appearing first in follicles at the primary-secondary transition. Quiescent oocytes within primordial follicles and primary follicles did not stain for SAS1B. Examination of neonatal rat ovaries revealed SAS1B expression first as faint signals in postnatal day 3 oocytes, with SAS1B protein staining intensifying with oocyte growth. Irrespective of animal age or estrus stage, SAS1B was seen only in oocytes of follicles that initiated a second granulosa cell layer. The precise temporal and spatial o</pubmed_abstract><journal>Developmental dynamics : an official publication of the American Association of Anatomists</journal><pubmed_title>SAS1B protein [ovastacin] shows temporal and spatial restriction to oocytes in several eutherian orders and initiates translation at the primary to secondary follicle transition.</pubmed_title><pmcid>PMC4091973</pmcid><funding_grant_id>U01HD60491-2S1</funding_grant_id><funding_grant_id>P51OD010425</funding_grant_id><funding_grant_id>U01 HD060491</funding_grant_id><funding_grant_id>D43TW/HD00654</funding_grant_id><funding_grant_id>UL1 TR000423</funding_grant_id><funding_grant_id>R01 HD035523</funding_grant_id><funding_grant_id>U54 HD029099</funding_grant_id><funding_grant_id>D43 TW000654</funding_grant_id><funding_grant_id>P51 OD010425</funding_grant_id><funding_grant_id>R03 HD055129</funding_grant_id><pubmed_authors>Flickinger C</pubmed_authors><pubmed_authors>Herr JC</pubmed_authors><pubmed_authors>Curnow E</pubmed_authors><pubmed_authors>Hlavin C</pubmed_authors><pubmed_authors>Mandal A</pubmed_authors><pubmed_authors>Klotz K</pubmed_authors><pubmed_authors>Shetty J</pubmed_authors><pubmed_authors>Ishola-Gbenla K</pubmed_authors><pubmed_authors>Macnamara E</pubmed_authors><pubmed_authors>Chertihin O</pubmed_authors><pubmed_authors>Khole A</pubmed_authors><pubmed_authors>Doerwaldt C</pubmed_authors><pubmed_authors>Herr AK</pubmed_authors><pubmed_authors>Chamberlain C</pubmed_authors><pubmed_authors>Feldman SH</pubmed_authors><pubmed_authors>Pires ES</pubmed_authors></additional><is_claimable>false</is_claimable><name>SAS1B protein [ovastacin] shows temporal and spatial restriction to oocytes in several eutherian orders and initiates translation at the primary to secondary follicle transition.</name><description>&lt;h4>Background&lt;/h4>Sperm Acrosomal SLLP1 Binding (SAS1B) protein (ovastacin) is an oolemmal binding partner for the intra-acrosomal sperm protein SLLP1.&lt;h4>Results&lt;/h4>Immunohistochemical localization revealed that SAS1B translation is restricted among adult tissues to the ovary and oocytes, SAS1B appearing first in follicles at the primary-secondary transition. Quiescent oocytes within primordial follicles and primary follicles did not stain for SAS1B. Examination of neonatal rat ovaries revealed SAS1B expression first as faint signals in postnatal day 3 oocytes, with SAS1B protein staining intensifying with oocyte growth. Irrespective of animal age or estrus stage, SAS1B was seen only in oocytes of follicles that initiated a second granulosa cell layer. The precise temporal and spatial o</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Dec</publication><modification>2025-04-04T19:24:12.968Z</modification><creation>2019-06-06T13:00:47Z</creation></dates><accession>S-EPMC4091973</accession><cross_references><pubmed>24038607</pubmed><doi>10.1002/dvdy.24040</doi></cross_references></HashMap>