Increased enhancer E2 function is insufficient to overcome endogenous mechanisms to repress <i>Klf4</i> in EpiLCs.

<p>mESCs with endogenous enhancer E2 mutations from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0311120#pone.0311120.g004" target="_blank">Fig 4</a> were converted to EpiLCs by growth in EpiLC induction media for 48 hours. Total RNA was...

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التفاصيل البيبلوغرافية
المؤلف الرئيسي:	Jack B. Waite (19762178) (author)
مؤلفون آخرون:	RuthMabel Boytz (19762181) (author), Alexis R. Traeger (19762184) (author), Torrey M. Lind (19762187) (author), Koya Lumbao-Conradson (19762190) (author), Sharon E. Torigoe (19762193) (author)
منشور في:	2024
الموضوعات:	Biophysics Biochemistry Cell Biology Neuroscience Developmental Biology Cancer Mental Health Infectious Diseases Computational Biology Space Science identify grammatical constraints expression upon loss div >< p state specific gene state specific function state specific activities stat3 binding sites direct enhancer activity sox2 binding site transcription factors oct4 binding sites specific states specific functions naïve state work suggests suboptimal oct4 spatiotemporal control reporter assays klf4 </ enhancer grammar enhancer e2 endogenous mutations critical functions biochemical tests also observed
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Increased enhancer E2 function is insufficient to overcome endogenous mechanisms to repress <i>Klf4</i> in EpiLCs.

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