PMID- 10872274 OWN - NLM STAT- MEDLINE DCOM- 20000727 LR - 20091109 IS - 0350-199X (Linking) VI - 54 IP - 1 DP - 2000 TI - [Molecular mechanisms in apoptosis]. PG - 33-40 AB - Apoptosis is evolutionary conserved form of cell suicide. Tumor necrosis factor-alpha (TNF-alpha) or Fas Ligand activated apoptosis by binding of the plasma membrane receptor. The activation of TNF Receptor 1 or Fas-Ligand Receptor lead to activate of caspase 8. The activation of the caspase-8 lead to activate the cell-death machinery cascade. The inhibitor of cell death machinery is Bcl-2 also fails to prevent Bax-induced cytochrome c release, activation of caspase-3, membrane blebbing, nuclear fragmentation, and cell death. Bcl-2 is important cell live-death regulator. Cleavage of specific protein subsets is a key event in the execution of apoptosis. Protein degradation may serve for the structural alterations in the process of cell self-destruction, but it may also function as a switch in the decisions between apoptosis and necrosis or apoptosis and cell proliferation. FAU - Habibovic, S AU - Habibovic S AD - Krankenhaus Sachsenhausen, Frauenklinik, Frankfurt, Germany. FAU - Hrgovic, Z AU - Hrgovic Z FAU - Bukvic, I AU - Bukvic I FAU - Hrgovic, I AU - Hrgovic I LA - hrv PT - English Abstract PT - Journal Article PT - Review TT - Molekularni mehanizmi kod apoptoze. PL - Bosnia and Herzegovina TA - Med Arh JT - Medicinski arhiv JID - 0400722 RN - 0 (Cytochrome c Group) RN - 0 (Proto-Oncogene Proteins c-bcl-2) RN - 0 (Tumor Necrosis Factor-alpha) RN - EC 3.4.22.- (Caspases) SB - IM MH - Animals MH - Apoptosis/*physiology MH - Caspases/physiology MH - Cytochrome c Group/physiology MH - Humans MH - Proto-Oncogene Proteins c-bcl-2/physiology MH - Tumor Necrosis Factor-alpha/physiology RF - 83 EDAT- 2000/06/29 11:00 MHDA- 2000/08/01 11:00 CRDT- 2000/06/29 11:00 PHST- 2000/06/29 11:00 [pubmed] PHST- 2000/08/01 11:00 [medline] PHST- 2000/06/29 11:00 [entrez] PST - ppublish SO - Med Arh. 2000;54(1):33-40.