1,721,083 research outputs found
Ca2(+) transfer from the ER to mitochondria: channeling cell death by a tumor suppressor.
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PARTICIPATION OF ENDOPLASMIC RETICULUM AND MITOCHONDRIAL CALCIUM HANDLING IN APOPTOSIS: MORE THAN JUST NEIGHBORHOOD?
No full textOver the past few years, extensive progress has been made in elucidating the role of calcium in the signaling of apoptosis. This has led to the characterization of calcium's role in the induction of apoptosis and in the regulation of effector proteases. In this review, we attempt to summarize the current knowledge regarding a segment of these studies, the interaction between the endoplasmic reticulum (ER) and mitochondria. This interface has been shown to play a crucial role in transferring agonist induced Ca2+ signals to mitochondria during physiological processes. Recent evidence, however, extended the role of this Ca2+ transfer to apoptotic pathways, showing that modulation of mitochondrial Ca2+ uptake from the ER side has a prominent role in modulating cellular fate
Transcriptional profiling of apoptosis: Cell death classification moves toward the systems era.
No full textSelective inhibition of potassium-stimulated rat adrenal glomerulosa cells by ruthenium red.
No full textChaperones as parts of organelle networks
No full textThe efficiency, divergence, and specificity of virtually all intracellular metabolic and signalling pathways largely depend on their compartmentalized organization. A corollary of the requirement of compartmentalization is the dynamic structural partition of the intracellular space by endomembrane systems. A branch of these membranes communicate with the extracellular space through the endo- and exocytotic processes. Others, like the mitochondrial and endoplasmic reticulum networks accomplish a further role, being fundamental for the maintenance of cellular energy balance and for determination of cell fate under stress conditions. Recent structural and functional studies revealed that the interaction of these networks and the connectivity state of mitochondria controls metabolic flow, protein transport, intracellular Ca2+ signalling, and cell death. Moreover, reflecting the fact that the above processes are accomplished in a microdomain between collaborating organelle membranes, the existence of macromolecular complexes at their contact sites have also been revealed. Being not only assistants of nascent protein folding, chaperones are proposed to participate in assembling and maintaining the function of the above complexes. In this chapter we discuss recently found examples of such an assembly of protein interactions driven by chaperone proteins, and their role in regulating physiological and pathological processes
The mitochondrial antioxidants MitoE(2) and MitoQ(10) increase mitochondrial Ca(2+) load upon cell stimulation by inhibiting Ca(2+) efflux from the organelle.
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