Loss of FAS/FASL signalling does not reduce apoptosis in Sharpin null mice.
Document Type
Article
Publication Date
9-2017
JAX Source
Exp Dermatol 2017 Sep; 26(9):820-822.
Volume
26
Issue
9
First Page
820
Last Page
822
ISSN
1600-0625
PMID
28094869
DOI
https://doi.org/10.1111/exd.13289
Grant
AR049288, CA034196
Abstract
Mice with mutations in SHANK-associated RH domain interactor (Sharpin) develop a hypereosinophilic auto-inflammatory disease known as chronic proliferative dermatitis. Affected mice have increased apoptosis in the keratinocytes of the skin, oesophagus and forestomach driven by extrinsic TNF receptor-mediated apoptotic signalling pathways. FAS receptor signalling is an extrinsic apoptotic signalling mechanism frequently involved in inflammatory skin diseases. Compound mutations in Sharpin and Fas or Fasl were created to determine whether these death domain proteins influenced the cutaneous phenotype in Sharpin null mice. Both Sharpin/Fas and Sharpin/Fasl compound mutant mice developed an auto-inflammatory phenotype similar to that seen in Sharpin null mice, indicating that initiation of apoptosis by FAS signalling is likely not involved in the pathogenesis of this disease. Exp Dermatol 2017 Sep; 26(9):820-822.
Recommended Citation
Potter C,
Silva K,
Kennedy VE,
Stearns T,
HogenEsch H,
Sundberg J.
Loss of FAS/FASL signalling does not reduce apoptosis in Sharpin null mice. Exp Dermatol 2017 Sep; 26(9):820-822.