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Wnt/β-Catenin Signaling Regulates Telomerase in Stem Cells and Cancer Cells

Authors: Hoffmeyer, K.; Angelo, R.; Rudloff, S.; Anton, R.; Hierholzer, A.; Del Valle, I.; Hein, K.; +2 Authors

Wnt/β-Catenin Signaling Regulates Telomerase in Stem Cells and Cancer Cells

Abstract

From Wnt Signals to Telomerase Activity Telomerase activity is associated with stem cell renewal and cancers, whereas a decrease in telomerase activity is seen during cell differentiation and senescence. Wnt/β-catenin signaling is also a critical regulator of stem cells, and deregulation of the pathway is associated with cancer. Now, Hoffmeyer et al. (p. 1549 ; see the Perspective by Greider ) have found a link between these two pathways. In embryonic stem cells, β-catenin was able to regulate telomerase expression and activity directly. Similar observations were obtained in adult stem cells, a model of intestinal tumors, and human cancer cells.

Keywords

Kruppel-Like Transcription Factors, Telomere Homeostasis, Telomere, Wnt Proteins, Adult Stem Cells, Kruppel-Like Factor 4, Mice, HEK293 Cells, Cell Line, Tumor, Neoplasms, Animals, Humans, RNA, Messenger, Transcription Initiation Site, Promoter Regions, Genetic, Telomerase, Wnt Signaling Pathway, Embryonic Stem Cells, beta Catenin

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Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
473
Top 1%
Top 1%
Top 0.1%