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Cited by 127

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Transient and Permanent Reconfiguration of Chromatin and Transcription Factor Occupancy Drive Reprogramming

Knaupp, Anja S., Buckberry, Sam, Pflueger, Jahnvi, Lim, Sue Mei, Ford, Ethan, Larcombe, Michael R., Rossello, Fernando J., de Mendoza, Alex, Alaei, Sara, Firas, Jaber, Holmes, Melissa L., Nair, Shalima S., Clark, Susan J., Nefzger, Christian M., Lister, Ryan, Polo, Jose M.·2017·Cell Stem Cell
DOI 10.1016/j.stem.2017.11.007
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  • In mouse embryonic fibroblasts (MEFs), OCT4 binds somatic enhancers during reprogramming and may initiate their inactivation, whereas in human fetal fibroblasts, OCT4 and SOX2 bind putative enhancers and remain bound in iPS cells.

    “Specifically, in mouse embryonic fibroblasts (MEFs), OCT4 binds somatic enhancers during reprogramming and may initiate their inactivation, whereas in human fetal fibroblasts, OCT4 and SOX2 bind putative enhancers and remain bound in iPS cells.”

    From Mechanisms, pathways and strategies for rejuvenation through epigenetic reprogramming (2023) · cites this paper as [81]

    The Discussion (page unavailable) reports Oct4/Sox2 binding at some regions open in MEFs, but it does not establish that Oct4 initiates somatic-enhancer inactivation; it says MEF enhancers can lose accessibility independently of Oct4/Sox2. The Introduction mentions human reprogramming studies, but our copy does not report the claimed persistent binding at putative enhancers in human fetal fibroblasts and their iPS cells. (LLM, conf=0.85)

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  • OSK factors interact with the genome and each other differently in mice than in human cells.

    “OSK factors interact with the genome and each other differently in mice than in human cells [80][81][82] , complicating the design and interpretation of studies.”

    From Mechanisms, pathways and strategies for rejuvenation through epigenetic reprogramming (2023) · cites this paper as [81]

    The Introduction (page not available) describes conflicting reports of OSK chromatin targeting in mouse and human reprogramming studies, supporting a reported difference in genome interactions. It does not establish a species-specific difference in how OSK factors interact with one another; the Discussion (page not available) also reports mouse results consistent with pioneer-factor activity, so the contrast is less settled than the claim suggests. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Early events in reprogramming are largely transient, so critical transitional OSKM-chromatin dynamics during such events are probably missing.

    “As the early events in reprogramming are largely transient 81 , we are probably missing critical transitional OSKM-chromatin dynamics during such events, leaving mechanistic questions largely unanswered.”

    From Mechanisms, pathways and strategies for rejuvenation through epigenetic reprogramming (2023) · cites this paper as [81]

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Research works printed but not linked: 38

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Metadata

Authors
Knaupp, A. S., Buckberry, S., Pflueger, J., Lim, S. M., Ford, E., Larcombe, M. R., Rossello, F. J., de Mendoza, A., Alaei, S., Firas, J., Holmes, M. L., Nair, S. S., Clark, S. J., Nefzger, C. M., Lister, R., & Polo, J. M.
Venue
Cell Stem Cell
Publisher
Elsevier BV
Published
2017-12
Volume
21
Issue
6
Pages
834-845.e6
ISSN
1934-5909
DOI
10.1016/j.stem.2017.11.007
Cited by
127
References
5
Language
en
Licence
Funders
  • National Health and Medical Research Council (NHMRC) of Australia (GNT1069830)
  • Australian Research Council (ARC) Centre of Excellence program in Plant Energy Biology (CE140100008)
  • ARC
  • Sylvia and Charles Viertel Senior Medical Research Fellowships
  • NHMRC CDF (APP1036587)
  • ARC Future Fellowship (FT120100862)
  • Howard Hughes Medical Institute International Research Scholarship
  • NHMRC-ARC Dementia Research Development Fellowship (APP1111206)
  • NHMRC Early Career Fellowship (APP1092280)

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