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Promoter directionality is controlled by U1 snRNP and polyadenylation signals

Author

Listed:
  • Albert E. Almada

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
    Massachusetts Institute of Technology)

  • Xuebing Wu

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
    Computational and Systems Biology Graduate Program, Massachusetts Institute of Technology)

  • Andrea J. Kriz

    (Massachusetts Institute of Technology)

  • Christopher B. Burge

    (Massachusetts Institute of Technology
    Computational and Systems Biology Graduate Program, Massachusetts Institute of Technology)

  • Phillip A. Sharp

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
    Massachusetts Institute of Technology)

Abstract

Asymmetric sequence determinants flanking gene transcription start sites are shown to control directionality of transcription elongation in mammalian cells by regulating promoter-proximal cleavage and polyadenylation.

Suggested Citation

  • Albert E. Almada & Xuebing Wu & Andrea J. Kriz & Christopher B. Burge & Phillip A. Sharp, 2013. "Promoter directionality is controlled by U1 snRNP and polyadenylation signals," Nature, Nature, vol. 499(7458), pages 360-363, July.
    • Handle: RePEc:nat:nature:v:499:y:2013:i:7458:d:10.1038_nature12349
    DOI: 10.1038/nature12349
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    Cited by:

    1. Amy L. Hughes & Aleksander T. Szczurek & Jessica R. Kelley & Anna Lastuvkova & Anne H. Turberfield & Emilia Dimitrova & Neil P. Blackledge & Robert J. Klose, 2023. "A CpG island-encoded mechanism protects genes from premature transcription termination," Nature Communications, Nature, vol. 14(1), pages 1-19, December.
    2. Xavier Contreras & David Depierre & Charbel Akkawi & Marina Srbic & Marion Helsmoortel & Maguelone Nogaret & Matthieu LeHars & Kader Salifou & Alexandre Heurteau & Olivier Cuvier & Rosemary Kiernan, 2023. "PAPĪ³ associates with PAXT nuclear exosome to control the abundance of PROMPT ncRNAs," Nature Communications, Nature, vol. 14(1), pages 1-14, December.

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