1,721,389 research outputs found
Calcium mobilization from mitochondria in synaptic transmitter release.
No full textMitochondria can rapidly accumulate and release Ca2+ upon cell stimulation. A paper by Yang and coworkers in this issue reports an unusual form of synaptic potentiation, dependent on Ca2+ release from mitochondria through the Na+/Ca2+ exchanger and triggered by Na+ entry through voltage-gated channels (Yang et al., 2003)
The collagen-mitochondria connection.
No full textA new study shows that mutations in Col6a, encoding collagen VI, cause muscle degeneration by affecting a distant target, the mitochondrion. The results show how elucidating the cellular consequences of genetic defects may provide unexpected perspectives into disease mechanism
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
Microdomains of intracellular Ca2+: molecular determinants and functional consequences.
No full textCalcium ions are ubiquitous and versatile signaling molecules, capable of decoding a variety of extracellular stimuli (hormones, neurotransmitters, growth factors, etc.) into markedly different intracellular actions, ranging from contraction to secretion, from proliferation to cell death. The key to this pleiotropic role is the complex spatiotemporal organization of the [Ca(2+)] rise evoked by extracellular agonists, which allows selected effectors to be recruited and specific actions to be initiated. In this review, we discuss the structural and functional bases that generate the subcellular heterogeneity in cellular Ca(2+) levels at rest and under stimulation. This complex choreography requires the concerted action of many different players; the central role is, of course, that of the calcium ion, with the main supporting characters being all the entities responsible for moving Ca(2+) between different compartments, while the cellular architecture provides a determining framework within which all the players have their exits and their entrances. In particular, we concentrate on the molecular mechanisms that lead to the generation of cytoplasmic Ca(2+) microdomains, focusing on their different subcellular location, mechanism of generation, and functional role
Microdomains of intracellular Ca2+: Molecular determinants and functional consequences
No full textCalcium ions are ubiquitous and versatile signaling molecules, capable of decoding a variety of extracellular stimuli (hormones, neurotransmitters, growth factors, etc.) into markedly different intracellular actions, ranging from contraction to secretion, from proliferation to cell death. The key to this pleiotropic role is the complex spatiotemporal organization of the [Ca(2+)] rise evoked by extracellular agonists, which allows selected effectors to be recruited and specific actions to be initiated. In this review, we discuss the structural and functional bases that generate the subcellular heterogeneity in cellular Ca(2+) levels at rest and under stimulation. This complex choreography requires the concerted action of many different players; the central role is, of course, that of the calcium ion, with the main supporting characters being all the entities responsible for moving Ca(2+) between different compartments, while the cellular architecture provides a determining framework within which all the players have their exits and their entrances. In particular, we concentrate on the molecular mechanisms that lead to the generation of cytoplasmic Ca(2+) microdomains, focusing on their different subcellular location, mechanism of generation, and functional role
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