Your browser doesn't support javascript.
loading
Wnt Signaling and Its Impact on Mitochondrial and Cell Cycle Dynamics in Pluripotent Stem Cells.
Rasmussen, Megan L; Ortolano, Natalya A; Romero-Morales, Alejandra I; Gama, Vivian.
Afiliación
  • Rasmussen ML; Department of Cell and Developmental Biology; Vanderbilt University, Nashville, TN37232, United States. megan.merolla@vanderbilt.edu.
  • Ortolano NA; Department of Cell and Developmental Biology; Vanderbilt University, Nashville, TN37232, United States. natalya.a.ortolano@vanderbilt.edu.
  • Romero-Morales AI; Department of Cell and Developmental Biology; Vanderbilt University, Nashville, TN37232, United States. a.romeromorales@vanderbilt.edu.
  • Gama V; Department of Cell and Developmental Biology; Vanderbilt University, Nashville, TN37232, United States. vivian.gama@vanderbilt.edu.
Genes (Basel) ; 9(2)2018 Feb 19.
Article en En | MEDLINE | ID: mdl-29463061
ABSTRACT
The core transcriptional network regulating stem cell self-renewal and pluripotency remains an intense area of research. Increasing evidence indicates that modified regulation of basic cellular processes such as mitochondrial dynamics, apoptosis, and cell cycle are also essential for pluripotent stem cell identity and fate decisions. Here, we review evidence for Wnt regulation of pluripotency and self-renewal, and its connections to emerging features of pluripotent stem cells, including (1) increased mitochondrial fragmentation, (2) increased sensitivity to cell death, and (3) shortened cell cycle. We provide a general overview of the stem cell-specific mechanisms involved in the maintenance of these uncharacterized hallmarks of pluripotency and highlight potential links to the Wnt signaling pathway. Given the physiological importance of stem cells and their enormous potential for regenerative medicine, understanding fundamental mechanisms mediating the crosstalk between Wnt, organelle-dynamics, apoptosis, and cell cycle will be crucial to gain insight into the regulation of stemness.
Palabras clave

Texto completo: 1 Banco de datos: MEDLINE Idioma: En Revista: Genes (Basel) Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Banco de datos: MEDLINE Idioma: En Revista: Genes (Basel) Año: 2018 Tipo del documento: Article País de afiliación: Estados Unidos