Biochemical and Biophysical Research Communications
Volume 268, Issue 2, 16 February 2000, Pages 243-248
Breakthroughs & ViewsRegulation of β-Catenin Signaling in the Wnt Pathway
References (75)
- et al.
Cell
(1992) - et al.
Cell
(1997) - et al.
Mech. Dev.
(1999) - et al.
Genomics
(1999) - et al.
Biochim. Biophys. Acta
(1992) - et al.
J. Biol. Chem.
(1999) - et al.
J. Biol. Chem.
(1999) Cell
(1994)- et al.
Cell
(1997) - et al.
Cell
(1997)
Curr. Biol.
(1998)
J. Biol. Chem.
(1998)
J. Biol. Chem.
(1999)
Biochim. Biophys. Acta
(1997)
J. Biol. Chem.
(1995)
Dev. Biol.
(1994)
Mech. Dev.
(1996)
Curr. Biol.
(1996)
J. Biol. Chem.
(1997)
Cell
(1998)
J. Biol. Chem.
(1999)
J. Biol. Chem.
(1999)
Cell
(1998)
Dev. Biol.
(1996)
Cell
(1997)
Genes Dev.
(1997)
Biochem. J.
(1998)
Genes Dev.
(1996)
J. Exp. Zool.
(1949)
Genet. Res.
(1984)
EMBO J.
(1998)
Mol. Cell. Biol.
(1998)
Science
(1998)
Science
(1999)
Development
(1999)
EMBO J.
(1990)
Nature
(1993)
Cited by (240)
Modulating MGMT expression through interfering with cell signaling pathways
2023, Biochemical PharmacologySignaling pathways in CRC
2021, Foundations of Colorectal CancerSilencing Celsr2 inhibits the proliferation and migration of Schwann cells through suppressing the Wnt/β-catenin signaling pathway
2020, Biochemical and Biophysical Research CommunicationsPTEN silencing enhances neuronal proliferation and differentiation by activating PI3K/Akt/GSK3β pathway in vitro
2018, Experimental Cell ResearchCitation Excerpt :The colony formation rates were 148 ± 7 and 380 ± 10 in PC12-sh-EGFP and PC12-sh-PTEN cells, and 60 ± 8 and 147 ± 11 in Neuro2A-sh-EGFP and Neuro2A-sh-PTEN (Fig. 2C and D). To confirm the results given above, cyclinD1 and c-Myc, which were important target genes of Wnt/β-catenin signaling pathway [37], were measured as makers of cell proliferation. Consistent with this, we found that PTEN knockdown resulted in up-regulation of the cyclinD1 and c-Myc at both mRNA and protein levels (Fig. 2E–G).
The Cell Cycle
2018, Physiology of the Gastrointestinal Tract, Sixth Edition
- 1
Fax: +81-82-257-5134. E-mail: [email protected].
Copyright © 2000 Published by Elsevier Inc. All rights reserved.