Açılan, CeydaYılmaz, Yusuf2021-10-212021-10-212011-08Ulukaya, E. vd. (2011).“Apoptosis: Why and how does it occur in biology?”. Cell Biochemistry and Function, 29(6), 468-480.0263-64841099-0844https://doi.org/10.1002/cbf.1774http://hdl.handle.net/11452/22428The literature on apoptosis has grown tremendously in recent years, and the mechanisms that are involved in this programmed cell death pathway have been enlightened. It is now known that apoptosis takes place starting from early development to adult stage for the homeostasis of multicellular organisms, during disease development and in response to different stimuli in many different systems. In this review, we attempted to summarize the current knowledge on the circumstances and the mechanisms that lead to induction of apoptosis, while going over the molecular details of the modulator and mediators of apoptosis as well as drawing the lines between programmed and non-programmed cell death pathways. The review will particularly focus on Bcl-2 family proteins, the role of different caspases in the process of apoptosis, and their inhibitors as well as the importance of apoptosis during different disease states. Understanding the molecular mechanisms involved in apoptosis better will make a big impact on human diseases, particularly cancer, and its management in the clinics.eninfo:eu-repo/semantics/closedAccessProgrammed cell deathApoptosisNecrosisApoptosis-inducing factors (Aifs)Caspaseinhibitor of apoptosis proteins (Iaps)Bcl-2 familyX-Linked inhibitorApo-1/Fas receptor/ligand systemCaspase-cleaved cytokeratin-18Bcl-2 family proteinsCells in-vitroFas-ligandCytochrome-CMitochondrial apoptosisChromosome-segregationBh3-only proteinsIntracisternal a-particlesApoptosisApoptosis inducing factorCaspasesHumansInhibitor of apoptosis proteinsNecrosisProto-Oncogene proteins c-bcl-2Signal transductionReview0002942671000052-s2.0-8005166869346848029621773978Biochemistry & molecular biologyCell biologyMitochondrial Membranes; Bcl-2; Bax Protein (53-86)2 morpholino 8 phenylchromoneAntineoplastic agentApoptosis inhibitörBAG 1 protein; BIM proteinCaspaseCaspase inhibitorCellular apoptosis susceptibility proteinCeramideFas antibodyFas associated death domain proteinGranzymeHLA DR3 antigenHLA DR4 antigenHLA DR5 antigenNavitoclaxNeuronal apoptosis inhibitory proteinNicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferaseObatoclaxPerforinProtein BADProtein baxProtein bcl 2Protein BidProtein kinase B inhibitorProtein p53SurvivinUnclassified drugUnindexed drugX linked inhibitor of apoptosisX linked inhibitor of apoptosis antagonistAcquired immune deficiency syndromeApoptosisCaenorhabditis elegansCancer chemotherapyCarcinogenesisCell activationCell cycleCell deathCell divisionCell growthCell protectionCell stressCell survivalCell swellingCytolysisCytotoxic T lymphocyteDephosphorylationDisease courseDNA damageDNA fragmentationDrug bindingDrug mechanismDrug synthesisEndometriumEnzyme activationEnzyme substrateEpstein barr virüsGenetic transcriptionHomeostasisHumanIn vitro studyInsulin dependent diabetes mellitusInternucleosomal DNA fragmentationKeratinocyteMitochondrial activationMitosisMolecular biologyMultiple sclerosisNatural killer cellNatural killer T cellNecrosisNeoplasmNerve cellNerve degenerationNonhumanOligomerizationOrgan transplantationOxidative stressPapilloma virüsPriority journalProtein cleavageProtein dephosphorylationProtein secretionReviewThymusUmor necrosis factor receptor associated periodic syndrome