000287483 001__ 287483
000287483 005__ 20240306154606.0
000287483 0247_ $$2doi$$a10.1038/s44320-024-00014-z
000287483 0247_ $$2pmid$$apmid:38302581
000287483 0247_ $$2altmetric$$aaltmetric:158951780
000287483 037__ $$aDKFZ-2024-00261
000287483 041__ $$aEnglish
000287483 082__ $$a570
000287483 1001_ $$0P:(DE-He78)a8af1162e07fdfa71acd30a8724af938$$aLim, Bryce$$b0$$eFirst author$$udkfz
000287483 245__ $$aCanalizing cell fate by transcriptional repression.
000287483 260__ $$aHeidelberg$$bEMBO Press$$c2024
000287483 3367_ $$2DRIVER$$aarticle
000287483 3367_ $$2DataCite$$aOutput Types/Journal article
000287483 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1709736318_31139$$xReview Article
000287483 3367_ $$2BibTeX$$aARTICLE
000287483 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000287483 3367_ $$00$$2EndNote$$aJournal Article
000287483 500__ $$aZMBH Alliance / #EA:A340#LA:A340# / 2024 Mar;20(3):144-161
000287483 520__ $$aPrecision in the establishment and maintenance of cellular identities is crucial for the development of multicellular organisms and requires tight regulation of gene expression. While extensive research has focused on understanding cell type-specific gene activation, the complex mechanisms underlying the transcriptional repression of alternative fates are not fully understood. Here, we provide an overview of the repressive mechanisms involved in cell fate regulation. We discuss the molecular machinery responsible for suppressing alternative fates and highlight the crucial role of sequence-specific transcription factors (TFs) in this process. Depletion of these TFs can result in unwanted gene expression and increased cellular plasticity. We suggest that these TFs recruit cell type-specific repressive complexes to their cis-regulatory elements, enabling them to modulate chromatin accessibility in a context-dependent manner. This modulation effectively suppresses master regulators of alternative fate programs and their downstream targets. The modularity and dynamic behavior of these repressive complexes enables a limited number of repressors to canalize and maintain major and minor cell fate decisions at different stages of development.
000287483 536__ $$0G:(DE-HGF)POF4-311$$a311 - Zellbiologie und Tumorbiologie (POF4-311)$$cPOF4-311$$fPOF IV$$x0
000287483 588__ $$aDataset connected to CrossRef, PubMed, , Journals: inrepo02.dkfz.de
000287483 650_7 $$2Other$$aAlternative Fate Repression
000287483 650_7 $$2Other$$aCell Fate Plasticity
000287483 650_7 $$2Other$$aCell Identity
000287483 650_7 $$2Other$$aEpigenetic Silencing
000287483 650_7 $$2Other$$aTranscriptional Repressor
000287483 7001_ $$aDomsch, Katrin$$b1
000287483 7001_ $$0P:(DE-He78)cb70d67b37a3b9239e352b7fbead37f5$$aMall, Moritz$$b2$$eLast author$$udkfz
000287483 7001_ $$00000-0002-0918-2758$$aLohmann, Ingrid$$b3
000287483 773__ $$0PERI:(DE-600)2193510-5$$a10.1038/s44320-024-00014-z$$n3$$p144-161$$tMolecular systems biology$$v20$$x1744-4292$$y2024
000287483 909CO $$ooai:inrepo02.dkfz.de:287483$$pVDB
000287483 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)a8af1162e07fdfa71acd30a8724af938$$aDeutsches Krebsforschungszentrum$$b0$$kDKFZ
000287483 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)cb70d67b37a3b9239e352b7fbead37f5$$aDeutsches Krebsforschungszentrum$$b2$$kDKFZ
000287483 9131_ $$0G:(DE-HGF)POF4-311$$1G:(DE-HGF)POF4-310$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vZellbiologie und Tumorbiologie$$x0
000287483 9141_ $$y2024
000287483 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bMOL SYST BIOL : 2022$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2021-07-19T13:27:40Z
000287483 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2021-07-19T13:27:40Z
000287483 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bDOAJ : Anonymous peer review, Double anonymous peer review$$d2021-07-19T13:27:40Z
000287483 915__ $$0LIC:(DE-HGF)CCBYNV$$2V:(DE-HGF)$$aCreative Commons Attribution CC BY (No Version)$$bDOAJ$$d2021-07-19T13:27:40Z
000287483 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bMOL SYST BIOL : 2022$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0561$$2StatID$$aArticle Processing Charges$$d2023-10-25
000287483 915__ $$0StatID:(DE-HGF)0700$$2StatID$$aFees$$d2023-10-25
000287483 9202_ $$0I:(DE-He78)A340-20160331$$kA340$$lA340 NWG Engeneering von Zellidentitäten und Krankheitsmodellen$$x0
000287483 9201_ $$0I:(DE-He78)A340-20160331$$kA340$$lA340 NWG Engeneering von Zellidentitäten und Krankheitsmodellen$$x0
000287483 9200_ $$0I:(DE-He78)A340-20160331$$kA340$$lA340 NWG Engeneering von Zellidentitäten und Krankheitsmodellen$$x0
000287483 980__ $$ajournal
000287483 980__ $$aVDB
000287483 980__ $$aI:(DE-He78)A340-20160331
000287483 980__ $$aUNRESTRICTED