Research summary
A synthesis of mitochondrial apoptosis pathways identified release of cytochrome c, changes in electron transport, loss of transmembrane potential, altered redox state, and Bcl-2 family protein actions as the central converging events, and outlined how upstream signals trigger or inhibit these events to define major physiological cell-death pathways [1]. Kinase Akt and p21-Ras were shown to phosphorylate pro-caspase-9 on serine-196; Akt-mediated phosphorylation inhibited Casp9 protease activity in vitro and in cells, while the Ser196Ala mutant was resistant to Akt-mediated phosphorylation and permitted Akt-resistant apoptosis induction [2]. The Inhibitor of Apoptosis (IAP) family, first discovered in baculoviruses, was reviewed as suppressors of host cell death during viral infection; ectopic expression of baculoviral IAPs blocked apoptosis triggered by diverse stimuli, framing IAPs as therapeutic targets for cancer, autoimmune disease and neurodegeneration [3]. Temperature-sensitive p53 in murine leukemia M1 cells induced temperature-dependent decreases in bcl-2 expression while increasing bax, and p53-deficient mice exhibited tissue-level increases in Bcl-2 and decreases in Bax, demonstrating that p53 regulates apoptosis at least in part through transcriptional control of bcl-2/bax [4]. Cytochrome c added to cell-free extracts activated caspases-2, -3, -6, -7, -8 and -10 in a caspase-9-dependent hierarchical cascade, while caspases-1, -4 and -5 were not activated; in vitro binding confirmed selective association of caspase-9 with Apaf-1 [5]. Apoptosis was demonstrated in myocardial samples from 36 cardiac-transplantation patients and three patients dying soon after myocardial infarction versus 11 normal controls, implicating programmed cell death in terminal heart failure [6]. Submicromolar recombinant Bax added to isolated mitochondria induced cytochrome c release, while a BH3 peptide alone was inactive; Bax plus mitochondria together activated caspases in purified cytosol, supporting a direct Bax channel function in cytochrome c release [7].
Recent publications
- Mitochondria and ApoptosisDOI
- An inhibitor of Bcl-2 family proteins induces regression of solid tumoursDOI
- Regulation of Cell Death Protease Caspase-9 by PhosphorylationDOI
- IAP family proteins---suppressors of apoptosisDOI
- Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo.
- ER stress-induced cell death mechanismsDOI
- Ordering the Cytochrome c鈥搃nitiated Caspase Cascade: Hierarchical Activation of Caspases-2, -3, -6, -7, -8, and -10 in a Caspase-9鈥揹ependent MannerDOI
- Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunitiesDOI
- Apoptosis in the Failing Human HeartDOI
- Bax directly induces release of cytochrome c from isolated mitochondriaDOI
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Email John C. Reed 6-12 months before your application deadline. Read several recent papers and reference specific work in your message. Use our how to email a Japanese professor guide for the proven email structure.
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External profiles
- ORCID: https://orcid.org/0009-0001-5364-3566
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, Kyushu University faculty directory). Last refreshed 2026-05. Report incorrect information.