Increased apoptosis in differentiating p27-deficient mouse embryonic stem cells

BRYJA, V., J. PACHERNÍK, K. SOUČEK, V. HORVATH, P. DVOŘÁK and Aleš HAMPL. Increased apoptosis in differentiating p27-deficient mouse embryonic stem cells. Cellular and molecular life sciences. 2004, vol. 61, No 11, p. 1384-1400. ISSN 1420-682X.

Basic information

Original name

Increased apoptosis in differentiating p27-deficient mouse embryonic stem cells

Authors

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

Edition

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

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Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

Genetics and molecular biology

Country of publisher

Switzerland

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 4.812

Organization unit

Faculty of Science

UT WoS

000221732300012

Keywords in English

stem cells

Tags

stem cells

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Abstract

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).