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SMAD4 mutations and cross-talk between TGF-β/IFNγ signaling accelerate rates of DNA damage and cellular senescence, resulting in a segmental progeroid syndrome—the Myhre syndrome

Crossref DOI link: https://doi.org/10.1007/s11357-020-00318-6

Published Online: 2021-01-05

Published Print: 2021-06

Update policy: https://doi.org/10.1007/springer_crossmark_policy

Authors

Kandhaya-Pillai, Renuka

Hou, Deyin

Zhang, Jiaming

Yang, Xiaomeng

Compoginis, Goli

Mori, Takayasu

Tchkonia, Tamara

Martin, George M.

Hisama, Fuki M.

Kirkland, James L.

Oshima, Junko https://orcid.org/0000-0001-5941-3799
Funding

Funding for this research was provided by:

Japan Society for the Promotion of Science London (17H04037)

National Institutes of Health (R01CA210916, R37AG013925, P01AG062413)

Robert and Arlene Kogod

A. Lindsay and Olive B. O'Connor Foundation

Robert J. and Theresa W. Ryan

the Noaber Foundation
License Information

Text and Data Mining valid from 2021-01-05

Version of Record valid from 2021-01-05
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Article History

Received: 18 September 2020

Accepted: 14 December 2020

First Online: 5 January 2021

Compliance with ethical standards

:

: The authors declare that they have no conflicts of interest.

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