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Positive intergenic...
Positive intergenic feedback circuitry, involving EBF1 and FOXO1, orchestrates B-cell fate
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- Mansson, Robert (författare)
- Karolinska Institutet,University of California, San Diego, USA
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- Welinder, Eva (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,University of California, San Diego, USA
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- Åhsberg, Josefine (författare)
- Linköpings universitet,Experimentell hematologi,Hälsouniversitetet
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- Lin, Yin C. (författare)
- University of California, San Diego, USA
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- Benner, Christopher (författare)
- University of California, San Diego, USA
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- Glass, Christopher K. (författare)
- University of California, San Diego, USA
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- Lucas, Joseph S. (författare)
- University of California, San Diego, USA
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- Sigvardsson, Mikael (författare)
- Linköpings universitet,Experimentell hematologi,Hälsouniversitetet
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- Murre, Cornelis (författare)
- University of California, San Diego, USA
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(creator_code:org_t)
- 2012-12-04
- 2012
- Engelska.
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 109:51, s. 21028-21033
- Relaterad länk:
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https://www.pnas.org...
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http://dx.doi.org/10...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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https://lup.lub.lu.s...
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http://kipublication...
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Abstract
Ämnesord
Stäng
- Recent studies have identified a number of transcriptional regulators, including E2A, early B-cell factor 1 (EBF1), FOXO1, and paired box gene 5 (PAX5), that promote early B-cell development. However, how this ensemble of regulators mechanistically promotes B-cell fate remains poorly understood. Here we demonstrate that B-cell development in FOXO1-deficient mice is arrested in the common lymphoid progenitor (CLP) LY6D(+) cell stage. We demonstrate that this phenotype closely resembles the arrest in B-cell development observed in EBF1-deficient mice. Consistent with these observations, we find that the transcription signatures of FOXO1- and EBF1-deficient LY6D(+) progenitors are strikingly similar, indicating a common set of target genes. Furthermore, we found that depletion of EBF1 expression in LY6D(+) CLPs severely affects FOXO1 mRNA abundance, whereas depletion of FOXO1 activity in LY6D(+) CLPs ablates EBF1 transcript levels. We generated a global regulatory network from EBF1 and FOXO1 genome-wide transcription factor occupancy and transcription signatures derived from EBF1- and FOXO1-deficient CLPs. This analysis reveals that EBF1 and FOXO1 act in a positive feedback circuitry to promote and stabilize specification to the B-cell lineage.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)
Nyckelord
- MEDICINE
- MEDICIN
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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