Involvement of MACH, a Novel MORT1/FADD-Interacting Protease, in Fas/APO-1- and TNF Receptor–Induced Cell Death
Open accessAbstract
Fas/APO-1 and p55 tumor necrosis factor (TNF) receptor (p55-R) activate cellular mechanisms that result in cell death. Upon activation of these receptors, Fas/APO-1 binds a protein called MORT1 (or FADD) and p55-R binds a protein called TRADD. MORT1 and TRADD can also bind to each other. We have cloned a novel protein, MACH, that binds to MORT1. This protein exists in multiple isoforms, some of which contain a region that has proteolytic activity and shows marked sequence homology to proteases of the ICE/CED-3 family. Cellular expression of the proteolytic MACH isoforms results in cell death. Expression of MACH isoforms that contain an incomplete ICE/CED-3 region provides effective protection against the cytotoxicity induced by Fas/APO-1 or p55-R triggering. These findings suggest that MACH is the most upstream enzymatic component in the Fas/APO-1- and p55-R-induced cell death signaling cascades.
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Death receptor ligation generally allows assembly of a dynamic multiprotein complex at the intracellular tail (DISC, complex I, complex II) that regulates CASP8 (or CASP10) activation.
“As a general rule, death receptor ligation allows for the assembly of a dynamic multiprotein complex at the intracellular tail of the receptor, such as so-called “death-inducing signaling complex” (DISC), “complex I”, and “complex II”, which operate as molecular platforms to regulate the activation and functions of CASP8 (or CASP10, in a limited number of settings) [274–276].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [274]
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References 58 · Cited by 2,292
- Authors
- Boldin, M. P., Goncharov, T. M., Goltseve, Y. V., & Wallach, D.
- Affiliations
- Weizmann Institute of Science (IL)
- Corresponding author
- Wallach, David
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1996-06
- Volume
- 85
- Issue
- 6
- Pages
- 803-815
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2032417513
- Cited by
- 2,292
- References
- 58
- Citations by year
- 2026: 16 · 2025: 15 · 2024: 20 · 2023: 21 · 2022: 22 · 2021: 31 · 2020: 8 · 2019: 18 · 2018: 23 · 2017: 24 · 2016: 21 · 2015: 19 · 2014: 39 · 2013: 36 · 2012: 34
- FWCI
- 100.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Weizmann Institute of Science
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- Mach, FADD, TRADD, Fas/APO-1, TNF receptor p55, apoptosis, cell death signaling, proteolytic activity, protein isoforms, death receptor signaling
- MeSH terms
- Amino Acid Sequence, Base Sequence, Carrier Proteins, Cell Line, Cloning, Molecular, Cysteine Endopeptidases, DNA-Binding Proteins, Humans, Kidney, Molecular Sequence Data, Organ Specificity, Protein Binding, Proteins, Recombinant Fusion Proteins, RNA, Messenger, Signal Transduction, Antigens, CD, Helminth Proteins, Apoptosis, Sequence Homology, Amino Acid, Receptors, Tumor Necrosis Factor, fas Receptor, Caspases, Caspase 1, Caenorhabditis elegans Proteins, Receptors, Tumor Necrosis Factor, Type I, TNF Receptor-Associated Factor 1, Adaptor Proteins, Signal Transducing, Fas-Associated Death Domain Protein
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