Controlling smad4 signaling with a wip

Author(s):
Dijke, P. ten (0000-0002-7234-342X); Baker, D.
Published
2020
Publication type
Other

Abstract

Members of the transforming growth factor-beta (TGF-beta) family play key roles in embryogenesis and in maintaining tissue homeostasis, and their perturbation can result in a broad range of diseases. One way TGF-beta family signaling pathways are kept in check is by reversible (de)phosphorylation of intracellular Smad effectors. In this issue of EMBO Reports, Park et al [1] identify the phosphatase wild-type p53-induced phosphatase 1 (Wip1) as a negative regulator of TGF-beta family signaling. Mechanistically, Wip1 constrains TGF-beta family signaling through direct dephosphorylation of Thr277, an activating MAP kinase phosphorylation site located in the linker region of the common mediator Smad4.

Date issued
2020-05-06
Language
English
Publisher
WILEY
hdl
1887/3182605
doi
10.15252/embr.202050246
URL
https://www.embopress.org/doi/full/10.15252/embr.202050246