Cleavage of RIP3 inactivates its caspase-independent apoptosis pathway by removal of kinase domain

Feng, Shanshan, Yang, Yonghui, Mei, Yide, Ma, Li, Zhu, De-e, Hoti, Naseruddin, Castanares, Mark, Wu, Mian·2007·Cellular Signalling

DOI 10.1016/j.cellsig.2007.05.016

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“Further, because FADD, RIPK1 (Zhang et al., 2011) and FADD, RIPK3 (Figure 1) DKO mice develop normally in utero, both RIPK1 and RIPK3 mediate embryonic lethality, most likely by the process of RIPK1RIPK3-mediated programmed necrosis (Weinlich et al., 2011).”
Result
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Authors: Feng, S., Yang, Y., Mei, Y., Ma, L., Zhu, D.-E., Hoti, N., Castanares, M., & Wu, M.
Venue: Cellular Signalling
Publisher: Elsevier BV
Published: 2007-10
Volume: 19
Issue: 10
Pages: 2056-2067
ISSN: 0898-6568 (ISSN-L)
DOI: 10.1016/j.cellsig.2007.05.016
OpenAlex: W2011698659
Cited by: 446
References: 0
FWCI: 2.16
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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Cleavage of RIP3 inactivates its caspase-independent apoptosis pathway by removal of kinase domain

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