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Functional specific roles of FADD: comparative proteomic analyses from knockout cell lines
Hongqin Zhuang1, Ziyi Gan, Weiwei Jiang
1The State Key Laboratory of Pharmaceutical Biotechnology, College of Life Science and School of Stomatology, Affiliated Stomatological Hospital, Nanjing University, Nanjing 210093, Jiangsu, PR China.
Molecular Biosystems
|May 22, 2013
Summary
Fas-associated death domain (FADD) protein influences cell death, proliferation, and survival. New research reveals FADD
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Fas-associated death domain (FADD) is a key adaptor protein in apoptosis.
- FADD also regulates cell proliferation and survival.
- Embryonic lethality in FADD-deficient mice is not due to apoptosis defects.
Purpose of the Study:
- To investigate the non-apoptotic roles of FADD.
- To identify proteins differentially expressed in FADD-deficient cells.
- To elucidate FADD's association with energy metabolism and proteolysis.
Main Methods:
- Proteomics identification of differentially-expressed proteins in FADD-deficient mouse embryonic fibroblasts (MEFs).
- Bioinformatic analyses, including network analysis using MetaCore™.
- Cell biology validation.
Main Results:
- 45 unique proteins were significantly altered in FADD-deficient MEFs.
- Dysregulated proteins were enriched in cellular metabolic processes (lipid metabolism, glycolysis, TCA cycle, oxidative phosphorylation).
- Enhanced fatty acid beta-oxidation and up-regulation of ubiquitin-proteasome pathway proteins were observed.
- c-Myc was identified as a central up-regulated hub.
Conclusions:
- FADD deficiency impacts energy metabolism and proteolysis, potentially causing embryonic lethality.
- Impaired mitochondrial function and proteolysis are implicated in FADD deficiency disorders.
- The link between FADD and cell metabolism offers insights into signaling pathway crosstalk.
