Increased apoptosis in differentiating p27-deficient mouse embryonic stem cells

BRYJA, V., J. PACHERNÍK, K. SOUČEK, V. HORVATH, P. DVOŘÁK a Aleš HAMPL. Increased apoptosis in differentiating p27-deficient mouse embryonic stem cells. Cellular and molecular life sciences. 2004, roč. 61, č. 11, s. 1384-1400. ISSN 1420-682X.

Základní údaje

Originální název

Increased apoptosis in differentiating p27-deficient mouse embryonic stem cells

Autoři

BRYJA, V., J. PACHERNÍK, K. SOUČEK, V. HORVATH, P. DVOŘÁK a Aleš HAMPL

Vydání

Cellular and molecular life sciences, 2004, 1420-682X

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Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

Genetika a molekulární biologie

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 4.812

Organizační jednotka

Přírodovědecká fakulta

UT WoS

000221732300012

Klíčová slova anglicky

stem cells

Štítky

stem cells

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Anotace

V originále

In mouse embryonic stem (mES) cells, the expression of p27 is elevated when differentiation is induced. Using mES cells lacking p27 we tested the importance of p27 for the regulation of three critical cellular processes: proliferation, differentiation, and apoptosis. Although cell cycle distribution, DNA synthesis, and the activity of key G1/S-regulating cyclin-dependent kinases remained unaltered in p27-deficient ES cells during retinoic acid-induced differentiation, the amounts of cyclin D2 and D3 in such cells were much lower compared with normal mES cells. The onset of differentiation induces apoptosis in p27-deficient cells, the extent of which can be reduced by artificially increasing the level of cyclin D3. We suggest that the role of p27 in at least some differentiation pathways of mES cells is to prevent apoptosis, and that it is not involved in slowing cell cycle progression. We also propose that the pro-survival function of p27 is realized via regulation of metabolism of D-type cyclin(s).