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RESEARCH PRODUCT
Apoptosis and the liver
Peter R. GalleStephan Kanzlersubject
Cancer ResearchProgrammed cell deathCeramideHepatitis Viral HumanDNA damageCellGenes mycApoptosisBiologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundmedicineHumansfas ReceptorLiver DiseasesLiver NeoplasmsIntrinsic apoptosisGenes p53Genes bcl-2Liver TransplantationCell biologymedicine.anatomical_structureLiverchemistryUVB-induced apoptosisApoptosisImmunologyPoly(ADP-ribose) PolymerasesSignal transductionReceptors Transforming Growth Factor betadescription
Regulation of the homeostatic balance between cell proliferation and programmed cell death, apoptosis, is essential for development and maintenance of multicellular organisms. Apoptosis is a genetically and evolutionarily highly conserved process. Analysis of the molecular mechanisms of apoptosis has led to a better understanding of many human diseases. Notably in cancer, but also in infectious or autoimmune disease, a deficiency in apoptosis is one of the key events in pathophysiology. On the other hand, overefficient apoptosis, as observed in fulminant liver failure, may be equally harmful for the organism indicating that a tight regulation of the apoptotic machinery is essential for survival. The execution of apoptosis may be initiated by many different signals, either from within or outside the cell involving ligand-receptor interactions, as has been shown for Fas/Fas-ligand, TNF-alpha/TNF-receptor or TGF-beta/TGF-receptor, or potentially by more unspecific signals such as ceramide or DNA damage. During the modulation phase of apoptosis many different genes such as p53, c-myc or Bcl-2/Bax have been shown to able to shift the balance either to cell survival or cell death.
year | journal | country | edition | language |
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2000-06-01 | Seminars in Cancer Biology |