- Abstract:
-
The retinoblastoma tumor suppressor protein pRb is a key regulator of cell cycle progression and mediator of the DNA damage response. Lysine methylation at K810, which occurs within a critical Cdk phosphorylation motif, holds pRb in the hypophosphorylated growth-suppressing state. We show here that methyl K810 is read by the tandem tudor domain containing tumor protein p53 binding protein 1 (53BP1). Structural elucidation of 53BP1 in complex with a methylated K810 pRb peptide emphasized the r...
Expand abstract - Publication status:
- Published
- Publisher copy:
- 10.1073/pnas.1403737111
-
Version unsuitable
-
We have not obtained a suitable full-text for a given research output. See this page for more information.
-
Recently completed
-
Sometimes content is held in ORA but is unavailable for a fixed period of time to comply with the policies and wishes of rights holders.
-
Permissions
-
All content made available in ORA should comply with relevant rights, such as copyright. See this page for more information.
-
Clearance
-
Some thesis volumes scanned as part of the digitisation scheme funded by Dr Leonard Polonsky are currently unavailable due to sensitive material or uncleared third-party copyright content. We are attempting to contact authors whose theses are affected.
- Publisher:
- National Academy of Sciences
- Journal:
- Proceedings of the National Academy of Sciences of the United States of America
- Volume:
- 111
- Issue:
- 31
- Pages:
- 11341-11346
- Publication date:
- 2014-08-05
- DOI:
- EISSN:
-
1091-6490
- ISSN:
-
0027-8424
- URN:
-
uuid:2e34d6cb-ab72-4f1b-b81f-4c2f264c7b29
- Source identifiers:
-
477014
- Local pid:
- pubs:477014
- Language:
- English
- Keywords:
- Copyright date:
- 2014
Journal article
Lysine methylation-dependent binding of 53BP1 to the pRb tumor suppressor.
Actions
Access Document
Why is the content I wish to access not available via ORA?
Bibliographic data (the information relating to research outputs) and full-text items (e.g. articles, theses, reports, etc.) arrive in ORA from several different sources. Unfortunately we are not able to make available the full-text for every research output.
Please contact the ORA team (
) if you have queries regarding unavailable content OR if you are aware of a full-text copy we can make available.
) if you have queries regarding unavailable content OR if you are aware of a full-text copy we can make available.
Content may be unavailable for the following four reasons
Alternative access to the full-text
You may be able to access the full-text directly from the publisher's website using the 'Publisher Copy' link in the 'Links & Downloads' box from a research output's ORA record page. This method may require an institutional or individual subscription to the journal/resource.
Authors
Bibliographic Details
Item Description
Terms of use
If you are the owner of this record, you can report an update to it here: Report update to this record