Matches in SemOpenAlex for { <https://semopenalex.org/work/W2025804527> ?p ?o ?g. }
- W2025804527 endingPage "2268" @default.
- W2025804527 startingPage "2257" @default.
- W2025804527 abstract "The morphogenesis of the hemochorial placenta is dependent upon the precise expansion and differentiation of trophoblast stem (TS) cells. SATB homeobox 1 (SATB1) and SATB2 are related proteins that have been implicated as regulators of some stem cell populations. SATB1 is highly expressed in TS cells, which prompted an investigation of SATB1 and the related SATB2 as regulators of TS cells. SATB1 and SATB2 were highly expressed in rat TS cells maintained in the stem state and rapidly declined following induction of differentiation. SATB proteins were also present within the rat placenta during early stages of its morphogenesis and disappeared as gestation advanced. Silencing Satb1 or Satb2 expression decreased TS cell self-renewal and increased differentiation, whereas ectopic expression of SATB proteins promoted TS cell expansion and blunted differentiation. Eomes, a key transcriptional regulator of TS cells, was identified as a target for SATB proteins. SATB knockdown decreased Eomes transcript levels and promoter activity, whereas SATB ectopic expression increased Eomes transcript levels and promoter activity. Electrophoretic mobility shift assay as well as chromatin immunoprecipitation analyses demonstrated that SATB proteins physically associate with a regulatory site within the Eomes promoter. We conclude that SATB proteins promote TS cell renewal and inhibit differentiation. These actions are mediated in part by regulating the expression of the TS cell stem-associated transcription factor, EOMES. The morphogenesis of the hemochorial placenta is dependent upon the precise expansion and differentiation of trophoblast stem (TS) cells. SATB homeobox 1 (SATB1) and SATB2 are related proteins that have been implicated as regulators of some stem cell populations. SATB1 is highly expressed in TS cells, which prompted an investigation of SATB1 and the related SATB2 as regulators of TS cells. SATB1 and SATB2 were highly expressed in rat TS cells maintained in the stem state and rapidly declined following induction of differentiation. SATB proteins were also present within the rat placenta during early stages of its morphogenesis and disappeared as gestation advanced. Silencing Satb1 or Satb2 expression decreased TS cell self-renewal and increased differentiation, whereas ectopic expression of SATB proteins promoted TS cell expansion and blunted differentiation. Eomes, a key transcriptional regulator of TS cells, was identified as a target for SATB proteins. SATB knockdown decreased Eomes transcript levels and promoter activity, whereas SATB ectopic expression increased Eomes transcript levels and promoter activity. Electrophoretic mobility shift assay as well as chromatin immunoprecipitation analyses demonstrated that SATB proteins physically associate with a regulatory site within the Eomes promoter. We conclude that SATB proteins promote TS cell renewal and inhibit differentiation. These actions are mediated in part by regulating the expression of the TS cell stem-associated transcription factor, EOMES." @default.
- W2025804527 created "2016-06-24" @default.
- W2025804527 creator A5000545378 @default.
- W2025804527 creator A5014344416 @default.
- W2025804527 creator A5023764322 @default.
- W2025804527 creator A5052804381 @default.
- W2025804527 creator A5069136549 @default.
- W2025804527 creator A5075519418 @default.
- W2025804527 creator A5078106567 @default.
- W2025804527 creator A5082285133 @default.
- W2025804527 date "2012-01-01" @default.
- W2025804527 modified "2023-09-30" @default.
- W2025804527 title "SATB Homeobox Proteins Regulate Trophoblast Stem Cell Renewal and Differentiation" @default.
- W2025804527 cites W1547855212 @default.
- W2025804527 cites W1569314672 @default.
- W2025804527 cites W1590367258 @default.
- W2025804527 cites W1641228030 @default.
- W2025804527 cites W1964886835 @default.
- W2025804527 cites W1970062529 @default.
- W2025804527 cites W1970925951 @default.
- W2025804527 cites W1971582979 @default.
- W2025804527 cites W1975751233 @default.
- W2025804527 cites W1984249881 @default.
- W2025804527 cites W1986651658 @default.
- W2025804527 cites W1988294855 @default.
- W2025804527 cites W1990718295 @default.
- W2025804527 cites W1992534873 @default.
- W2025804527 cites W1994115491 @default.
- W2025804527 cites W1994144105 @default.
- W2025804527 cites W1997263143 @default.
- W2025804527 cites W1998498869 @default.
- W2025804527 cites W2004102023 @default.
- W2025804527 cites W2004232360 @default.
- W2025804527 cites W2006779861 @default.
- W2025804527 cites W2012305943 @default.
- W2025804527 cites W2013856253 @default.
- W2025804527 cites W2017756762 @default.
- W2025804527 cites W2021170422 @default.
- W2025804527 cites W2022306286 @default.
- W2025804527 cites W2026399748 @default.
- W2025804527 cites W2027200579 @default.
- W2025804527 cites W2031675290 @default.
- W2025804527 cites W2032206017 @default.
- W2025804527 cites W2033861867 @default.
- W2025804527 cites W2041695960 @default.
- W2025804527 cites W2043980237 @default.
- W2025804527 cites W2045899482 @default.
- W2025804527 cites W2046165140 @default.
- W2025804527 cites W2049460839 @default.
- W2025804527 cites W2050603927 @default.
- W2025804527 cites W2056312662 @default.
- W2025804527 cites W2057159461 @default.
- W2025804527 cites W2060441220 @default.
- W2025804527 cites W2064967147 @default.
- W2025804527 cites W2066329598 @default.
- W2025804527 cites W2069977787 @default.
- W2025804527 cites W2087984111 @default.
- W2025804527 cites W2088237277 @default.
- W2025804527 cites W2089285124 @default.
- W2025804527 cites W2094706459 @default.
- W2025804527 cites W2098094337 @default.
- W2025804527 cites W2105244370 @default.
- W2025804527 cites W2105469909 @default.
- W2025804527 cites W2106372318 @default.
- W2025804527 cites W2111024053 @default.
- W2025804527 cites W2112980664 @default.
- W2025804527 cites W2114436231 @default.
- W2025804527 cites W2115235864 @default.
- W2025804527 cites W2123829995 @default.
- W2025804527 cites W2127311430 @default.
- W2025804527 cites W2129114889 @default.
- W2025804527 cites W2132069716 @default.
- W2025804527 cites W2138417516 @default.
- W2025804527 cites W2142303444 @default.
- W2025804527 cites W2143137932 @default.
- W2025804527 cites W2156475356 @default.
- W2025804527 cites W2157494005 @default.
- W2025804527 cites W2158487422 @default.
- W2025804527 cites W2169529166 @default.
- W2025804527 cites W4238567307 @default.
- W2025804527 doi "https://doi.org/10.1074/jbc.m111.287128" @default.
- W2025804527 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3265903" @default.
- W2025804527 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22123820" @default.
- W2025804527 hasPublicationYear "2012" @default.
- W2025804527 type Work @default.
- W2025804527 sameAs 2025804527 @default.
- W2025804527 citedByCount "50" @default.
- W2025804527 countsByYear W20258045272012 @default.
- W2025804527 countsByYear W20258045272013 @default.
- W2025804527 countsByYear W20258045272014 @default.
- W2025804527 countsByYear W20258045272015 @default.
- W2025804527 countsByYear W20258045272016 @default.
- W2025804527 countsByYear W20258045272017 @default.
- W2025804527 countsByYear W20258045272018 @default.
- W2025804527 countsByYear W20258045272019 @default.
- W2025804527 countsByYear W20258045272020 @default.
- W2025804527 countsByYear W20258045272021 @default.
- W2025804527 countsByYear W20258045272022 @default.