BRYJA, V., J. PACHERNÍK, L. FALDÍKOVÁ, P. KREJČÍ, R. POGUE, I. NEVŘIVÁ, P. DVOŘÁK and Aleš HAMPL. The role of p27(Kip1) in maintaining the levels of D-type cyclins in vivo. Biochimica et Biophysica Acta. 2004, vol. 1691, 2-3, p. 105-116. ISSN 0006-3002.
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Basic information
Original name The role of p27(Kip1) in maintaining the levels of D-type cyclins in vivo
Authors BRYJA, V., J. PACHERNÍK, L. FALDÍKOVÁ, P. KREJČÍ, R. POGUE, I. NEVŘIVÁ, P. DVOŘÁK and Aleš HAMPL.
Edition Biochimica et Biophysica Acta, 2004, 0006-3002.
Other information
Original language English
Type of outcome Article in a journal
Field of Study Genetics and molecular biology
Country of publisher Netherlands
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 2.590 in 1999
Organization unit Faculty of Science
UT WoS 000221211800004
Keywords in English cells
Tags cells
Changed by Changed by: prof. Mgr. Vítězslav Bryja, Ph.D., učo 11088. Changed: 8/7/2009 10:54.
Abstract
This in vivo study employs p27-deficient mice to investigate the significance of p27 for the metabolism of D-type cyclins in differentiated cells. The absence of p27 results in decreased levels of cyclins D2 and/or D3 in some organs. As demonstrated on Leydig cells of testis, such dependency is only restricted to certain cell types including terminally differentiated ones, and the absence of p27 in these cells can interfere with their differentiation. The decrease of cyclin D caused by the absence of p27 equals the amount of cyclin D physically associated with p27 in non-mutant animals. The data indicate that it is the proportion of p27-associated cyclin D that determines the response to p27 deficiency. Cells in which the level of D-type cyclin is dependent on p27 do not up-regulate the activity of their CDK2 and CDK4 upon loss of p27, and these cells have a negligible amount of p27 bound to CDK2 and/or cyclin A/E under normal conditions. Together, the findings suggest the existence of a dual role for p27, one being a classical regulation of cell cycle via inhibition of cyclin-dependent kinases (CDK), and the other being participation in the establishment and/or maintenance of differentiated status that is realized in conjunction with D-type cyclins.
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