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p205, A potential tumor suppressor, inhibits cell proliferation via multiple pathways of cell cycle regulation

Asefa, Benyam ; Dermott, Jonathan M. ; Kaldis, Philipp LU orcid ; Stefanisko, Karen ; Garfinkel, David J. and Keller, Jonathan R. (2006) In FEBS Letters 580(5). p.1205-1214
Abstract

p205 is a member of the interferon-inducible p200 family of proteins that regulate cell proliferation. Over-expression of p205 inhibits cell growth, although its mechanism of action is currently unknown. Therefore, we evaluated the effect of p205 on the p53 and Rb-dependent pathways of cell cycle regulation. p205 expression results in elevated levels of p21, and activates the p21 promoter in vitro in a p53-dependent manner. In addition, p205 induces increased expression of Rb, and binds directly to Rb and p53. Interestingly, p205 also induces growth inhibition independent of p53 and Rb by delaying G2/M progression in proliferating cells, and is a substrate for Cdk2 kinase activity. Finally, we have identified other binding partners of... (More)

p205 is a member of the interferon-inducible p200 family of proteins that regulate cell proliferation. Over-expression of p205 inhibits cell growth, although its mechanism of action is currently unknown. Therefore, we evaluated the effect of p205 on the p53 and Rb-dependent pathways of cell cycle regulation. p205 expression results in elevated levels of p21, and activates the p21 promoter in vitro in a p53-dependent manner. In addition, p205 induces increased expression of Rb, and binds directly to Rb and p53. Interestingly, p205 also induces growth inhibition independent of p53 and Rb by delaying G2/M progression in proliferating cells, and is a substrate for Cdk2 kinase activity. Finally, we have identified other binding partners of p205 by a yeast two-hybrid screen, including the paired homeodomain protein HoxB2. Taken together, our results indicate that p205 induces growth arrest by interaction with multiple transcription factors that regulate the cell cycle, including but not entirely dependent on the Rb- and p53-mediated pathways of growth inhibition.

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author
; ; ; ; and
publishing date
type
Contribution to journal
publication status
published
keywords
Cell cycle regulation, Interferon-inducible, p205, p21, p53, Rb
in
FEBS Letters
volume
580
issue
5
pages
1205 - 1214
publisher
Wiley-Blackwell
external identifiers
  • pmid:16458891
  • scopus:32344439914
ISSN
0014-5793
DOI
10.1016/j.febslet.2006.01.032
language
English
LU publication?
no
id
17334e7d-4a53-461d-922f-346f1a0d7cc7
date added to LUP
2019-09-18 14:24:54
date last changed
2024-01-01 20:41:03
@article{17334e7d-4a53-461d-922f-346f1a0d7cc7,
  abstract     = {{<p>p205 is a member of the interferon-inducible p200 family of proteins that regulate cell proliferation. Over-expression of p205 inhibits cell growth, although its mechanism of action is currently unknown. Therefore, we evaluated the effect of p205 on the p53 and Rb-dependent pathways of cell cycle regulation. p205 expression results in elevated levels of p21, and activates the p21 promoter in vitro in a p53-dependent manner. In addition, p205 induces increased expression of Rb, and binds directly to Rb and p53. Interestingly, p205 also induces growth inhibition independent of p53 and Rb by delaying G2/M progression in proliferating cells, and is a substrate for Cdk2 kinase activity. Finally, we have identified other binding partners of p205 by a yeast two-hybrid screen, including the paired homeodomain protein HoxB2. Taken together, our results indicate that p205 induces growth arrest by interaction with multiple transcription factors that regulate the cell cycle, including but not entirely dependent on the Rb- and p53-mediated pathways of growth inhibition.</p>}},
  author       = {{Asefa, Benyam and Dermott, Jonathan M. and Kaldis, Philipp and Stefanisko, Karen and Garfinkel, David J. and Keller, Jonathan R.}},
  issn         = {{0014-5793}},
  keywords     = {{Cell cycle regulation; Interferon-inducible; p205; p21; p53; Rb}},
  language     = {{eng}},
  month        = {{02}},
  number       = {{5}},
  pages        = {{1205--1214}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{FEBS Letters}},
  title        = {{p205, A potential tumor suppressor, inhibits cell proliferation via multiple pathways of cell cycle regulation}},
  url          = {{http://dx.doi.org/10.1016/j.febslet.2006.01.032}},
  doi          = {{10.1016/j.febslet.2006.01.032}},
  volume       = {{580}},
  year         = {{2006}},
}