BRYJA, V., J. PACHERNÍK, L. FALDÍKOVÁ, P. KREJČÍ, R. POGUE, I. NEVŘIVÁ, P. DVOŘÁK a Aleš HAMPL. The role of p27(Kip1) in maintaining the levels of D-type cyclins in vivo. Biochimica et Biophysica Acta. 2004, roč. 1691, 2-3, s. 105-116. ISSN 0006-3002.
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Základní údaje
Originální název The role of p27(Kip1) in maintaining the levels of D-type cyclins in vivo
Autoři BRYJA, V., J. PACHERNÍK, L. FALDÍKOVÁ, P. KREJČÍ, R. POGUE, I. NEVŘIVÁ, P. DVOŘÁK a Aleš HAMPL.
Vydání Biochimica et Biophysica Acta, 2004, 0006-3002.
Další údaje
Originální jazyk angličtina
Typ výsledku Článek v odborném periodiku
Obor Genetika a molekulární biologie
Stát vydavatele Nizozemské království
Utajení není předmětem státního či obchodního tajemství
Impakt faktor Impact factor: 2.590 v roce 1999
Organizační jednotka Přírodovědecká fakulta
UT WoS 000221211800004
Klíčová slova anglicky cells
Štítky cells
Změnil Změnil: prof. Mgr. Vítězslav Bryja, Ph.D., učo 11088. Změněno: 8. 7. 2009 10:54.
Anotace
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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