Functional complementation between FADD and RIP1 in embryos and lymphocytes

Haibing Zhang, Xiaohui Zhou, Thomas McQuade, Jinghe Li, Francis Ka-Ming Chan () and Jianke Zhang ()
Additional contact information
Haibing Zhang: Kimmel Cancer Center, Thomas Jefferson University
Xiaohui Zhou: Kimmel Cancer Center, Thomas Jefferson University
Thomas McQuade: University of Massachusetts Medical School
Jinghe Li: Kimmel Cancer Center, Thomas Jefferson University
Francis Ka-Ming Chan: University of Massachusetts Medical School
Jianke Zhang: Kimmel Cancer Center, Thomas Jefferson University

Nature, 2011, vol. 471, issue 7338, 373-376

Abstract: Shared function of FADD and RIPK1 Regulation of cell death is vital for embryonic development and homeostasis in somatic cells, and the Fas-associated death domain (FADD) is a critical signalling adaptor for extrinsic apoptotic pathways. In a study of potential interactions between FADD and receptor interacting protein kinase-1 (RIP1/RIPK1), double deficiency of FADD and RIPK1 is shown to rescue the defects in embryonic development and lymphocyte proliferation seen in mice with single gene deficiencies. This suggests that FADD (presumably in conjunction with caspase-8 and c-FLIP) keeps necrosis in check by causing cleavage of RIPK1.

Date: 2011
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/nature09878 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:471:y:2011:i:7338:d:10.1038_nature09878

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature09878

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().