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Another piece of the p27Kip1 puzzle

Kaldis, Philipp LU orcid (2007) In Cell 128(2). p.241-244
Abstract

How extracellular signals communicate with the cell cycle is poorly understood. In this issue, two papers (Grimmler et al., 2007; Chu et al., 2007) address this problem by reporting phosphorylation of the cyclin-dependent kinase inhibitor p27Kip1 on a tyrosine residue by nonreceptor tyrosine kinases, which decreases p27 stability. This new mechanism could explain how cells enter the cell cycle from a quiescent state.

Please use this url to cite or link to this publication:
author
publishing date
type
Contribution to journal
publication status
published
in
Cell
volume
128
issue
2
pages
241 - 244
publisher
Cell Press
external identifiers
  • pmid:17254963
  • scopus:33846330967
ISSN
0092-8674
DOI
10.1016/j.cell.2007.01.006
language
English
LU publication?
no
id
9846ea4e-c170-45f9-9955-b652461789cf
date added to LUP
2019-09-18 14:18:02
date last changed
2024-03-19 21:22:04
@article{9846ea4e-c170-45f9-9955-b652461789cf,
  abstract     = {{<p>How extracellular signals communicate with the cell cycle is poorly understood. In this issue, two papers (Grimmler et al., 2007; Chu et al., 2007) address this problem by reporting phosphorylation of the cyclin-dependent kinase inhibitor p27<sup>Kip1</sup> on a tyrosine residue by nonreceptor tyrosine kinases, which decreases p27 stability. This new mechanism could explain how cells enter the cell cycle from a quiescent state.</p>}},
  author       = {{Kaldis, Philipp}},
  issn         = {{0092-8674}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{2}},
  pages        = {{241--244}},
  publisher    = {{Cell Press}},
  series       = {{Cell}},
  title        = {{Another piece of the p27Kip1 puzzle}},
  url          = {{http://dx.doi.org/10.1016/j.cell.2007.01.006}},
  doi          = {{10.1016/j.cell.2007.01.006}},
  volume       = {{128}},
  year         = {{2007}},
}