Avtor/Urednik		Cirman, Tina
Naslov		Cepitev molekule Bid kot možni mehanizem sprožitve apoptoze z lizosomskimi cisteinskimi proteazami
Tip		monografija
Kraj izdaje		Ljubljana
Založnik		Univerza v Ljubljani, Medicinska fakulteta
Leto izdaje		2004
Obseg		str. 136
Jezik		slo
Abstrakt		Apoptosis is a programmed form of cell death, characterized by typical biochemical and morphological changes of an apoptotic cell. These changes are a consequence of cleavage of target proteins by cysteine proteases, caspases. Caspases are located in the cytosol as proenzymes and are activated upon apoptosis triggering via one of two major pathways. Binding of ligands to death receptors triggers extrinsic pathway, resulting in activation of initiator caspase-8. Activation of intrinsic (mitochondrial) pathway is a consequence of intracellular stress, resulting in cytochrome c release from mitochondria and activation of initiator caspase-9. Initiator caspases in turn activate executioner caspases-3, -6 and-7. Both pathways are connected via proapoptotic molecule form the Bcl-2 family of proteins, Bid. Bid is cleaved by activated caspase-8 and can - in its truncated form - trigger release of cytochrome c from mitochondria. Cathepsins are papain-like lysosomal cysteine proteases. Their activity is regulated on several levels - they are synthesyzed as proenzymes that are activated only in the acidic environment of lysosomes. Cathepsins are separated from the cytosol by lysosomal membrane, their activity in the neutral pH of cytosol is lower and are additionally inhibited by cystatins and other protease inhibitors. Cathepsins are important players of intralysosomal protein degradation but have also some very specific functions: they are participating in the rearrangement and resorption of the bones, processing of invariant cahin (Ii), maintaining epidermis homeostasis, processing of other proteins and prohormones and production of endostatins. Cathepsins also play a role in apoptosis that is triggered by their translocation from lysosomes to the cytosol. Such translocation is a consequence of decreased lysosomal stability, triggered by various insults lysosomotropic agents, reactive oxygen species, during ageing and in various pathological conditions.
Deskriptorji		APOPTOSIS CATHEPSINS CYSTEINE PROTEINASE INHIBITORS HELA CELLS TRANSFECTION DNA, COMPLEMENTARY BASE SEQUENCE POLYMERASE CHAIN REACTION CYTOCHROME C FLOW CYTOMETRY