Pluripotency and self-renewal of embryonic stem cells (ESCs) are maintained by regulatory mechanisms, based on a sophisticated network of transcription factors. Recently, a growing body of evidence has indicated that Klf5, a transcription factor highly expressed in mouse ESCs and during the early phases of mouse development, plays a crucial role in maintaining ESC self-renewal and pluripotency, in governing ESC fate decisions and proper development of blastocyst in vivo. Indeed, Klf5-null mice show developmental defects at blastocyst stage, due to the defective establishment of the inner cell mass. Moreover, Klf5 knockdown in ESCs results in the loss of undifferentiated phenotype, whereas its ectopic expression is sufficient to maintain ESC in the undifferentiated state, even in the absence of LIF. Finally, it has been recently reported that Klf5 activates the expression of self-renewal-promoting genes and, simultaneously, it inhibits the expression of differentiation-related genes. Here, we discuss the functional role of Klf5 in the control on ESC self-renewal and pluripotency and its integration in the core transcriptional network governing ESC state.

Regulatory role of Klf5 in early mouse development and in embryonic stem cells / Parisi, Silvia; Russo, Tommaso. - In: VITAMINS AND HORMONES. - ISSN 0083-6729. - 87:(2011), pp. 381-397. [10.1016/B978-0-12-386015-6.00037-8]

Regulatory role of Klf5 in early mouse development and in embryonic stem cells.

PARISI, SILVIA;RUSSO, TOMMASO
2011

Abstract

Pluripotency and self-renewal of embryonic stem cells (ESCs) are maintained by regulatory mechanisms, based on a sophisticated network of transcription factors. Recently, a growing body of evidence has indicated that Klf5, a transcription factor highly expressed in mouse ESCs and during the early phases of mouse development, plays a crucial role in maintaining ESC self-renewal and pluripotency, in governing ESC fate decisions and proper development of blastocyst in vivo. Indeed, Klf5-null mice show developmental defects at blastocyst stage, due to the defective establishment of the inner cell mass. Moreover, Klf5 knockdown in ESCs results in the loss of undifferentiated phenotype, whereas its ectopic expression is sufficient to maintain ESC in the undifferentiated state, even in the absence of LIF. Finally, it has been recently reported that Klf5 activates the expression of self-renewal-promoting genes and, simultaneously, it inhibits the expression of differentiation-related genes. Here, we discuss the functional role of Klf5 in the control on ESC self-renewal and pluripotency and its integration in the core transcriptional network governing ESC state.
2011
Regulatory role of Klf5 in early mouse development and in embryonic stem cells / Parisi, Silvia; Russo, Tommaso. - In: VITAMINS AND HORMONES. - ISSN 0083-6729. - 87:(2011), pp. 381-397. [10.1016/B978-0-12-386015-6.00037-8]
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/456667
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 19
  • ???jsp.display-item.citation.isi??? 16
social impact