BCL2-related ovarian killer (BOK) proteinak heriotza zelular programatuan eta mitokondrioen morfologiaren eraldaketan parte hartzen du
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BCL2 familiako proteinak heriotz zelular programatua (apoptosia) erregulatzen duten osagai zelular nagusiak dira. BCL2 familiako proteinak bi taldetan bana daitezke funtzioaren arabera: kide pro-apoptotikoak eta kide anti-apoptotikoak. Nahiz eta BOK orain dela ia bi hamarkada aurkitu zen, BCL2 familiako kideen arteko ezezagunenetako bat da. Kide pro-apoptotikoekin (BAX/BAK) zenbait antzekotasun erakusten dituenez, proteina pro-apoptotikoekin funtzionalki eta mekanistikoki errendundantea dela onartu izan da. Hala ere, uste hori zehazki egiaztatzear dago. Lan honetan, BOKek BAX/BAKekin ezaugarri komunak elkarbanatzeaz gain, desberdintasun garrantzitsuak dituela adierazten duten zenbait ebidentzia erakusten ditugu.
BCL2 family proteins are the main regulators of program cell death (apoptosis). Depending on their function, BCL2 proteins can be divided in two main groups: the pro-apoptotic members and the anti-apoptotic members. Although BOK was identified almost two decades ago, it remains as one of the least understood BCL2 family members. Because BOK present certain similarities with pro-apoptotic proteins (BAX/BAK), it has been often been assumed that BOK is functionally and mechanistically redundant with BAX/BAK. However, this assumption remains to be explicitly proven. Here, we present distinct lines of evidence indicating that the cellular behaviour of BOK shares some common features but also important differences with BAX/BAK. .
BCL2 family proteins are the main regulators of program cell death (apoptosis). Depending on their function, BCL2 proteins can be divided in two main groups: the pro-apoptotic members and the anti-apoptotic members. Although BOK was identified almost two decades ago, it remains as one of the least understood BCL2 family members. Because BOK present certain similarities with pro-apoptotic proteins (BAX/BAK), it has been often been assumed that BOK is functionally and mechanistically redundant with BAX/BAK. However, this assumption remains to be explicitly proven. Here, we present distinct lines of evidence indicating that the cellular behaviour of BOK shares some common features but also important differences with BAX/BAK. .
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Apoptosia, BCL2 familiako proteinak, mitokondrioen dinamika, minbizia, Apoptosis, BCL2 family proteins, mitochondrial dynamics, cancer