PMC . NCBI . NLM . NIH . GOV {
}
We are analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC2730423/.
Title:
Ca2+ transfer from the ER to mitochondria: when, how and why - PMC
Description:
The heterogenous subcellular distribution of a wide array of channels, pumps and exchangers allows extracellular stimuli to induce increases in cytoplasmic Ca2+ concentration ([Ca2+]c) with highly defined spatial and temporal patterns, that in turn ...
Website Age:
27 years and 8 months (reg. 1997-10-02).
Title:
Ca2+ transfer from the ER to mitochondria: when, how and why - PMC
Description:
The heterogenous subcellular distribution of a wide array of channels, pumps and exchangers allows extracellular stimuli to induce increases in cytoplasmic Ca2+ concentration ([Ca2+]c) with highly defined spatial and temporal patterns, that in turn ...
Website Age:
27 years and 8 months (reg. 1997-10-02).
Matching Content Categories {📚}
- Education
- Science
- Telecommunications
Content Management System {📝}
What CMS is pmc.ncbi.nlm.nih.gov built with?
Custom-built
No common CMS systems were detected on Pmc.ncbi.nlm.nih.gov, and no known web development framework was identified.
Traffic Estimate {📈}
What is the average monthly size of pmc.ncbi.nlm.nih.gov audience?
🌠 Phenomenal Traffic: 5M - 10M visitors per month
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How Does Pmc.ncbi.nlm.nih.gov Make Money? {💸}
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Keywords {🔍}
doi, pubmed, google, scholar, mitochondrial, cell, mitochondria, pmc, article, free, calcium, protein, bcl, cells, ipr, membrane, channel, vdac, release, apoptosis, role, molecular, journal, channels, inositol, biological, chemistry, endoplasmic, reticulum, opening, uptake, permeability, regulation, trisphosphate, biol, death, binding, signal, apoptotic, signaling, receptor, ptp, kinase, proteins, akt, mcu, phosphorylation, intracellular, transition, rizzuto,
Topics {✒️}
voltage-dependent anion-selective channel multi-domain pro-apoptotic subfamily transforming growth factor-beta er/mitochondrial ca2+ cross-talk armadillo-repeat protein structures voltage-dependent anion channel calmodulin-dependent protein kinaseii lower steady-state [ca2+]er weakly anion-selective channel ca2+-dependent calmodulin activation pmc beta search er/mitochondria ca2+ cross-talk heat-shock protein pbp74 cyclosporin a-sensitive channel ca2+-dependent dephosphorylation step agonist-sensitive internal store organelle-targeted aequorin probes sercoplasmic/endoplasmic calcium atpase coxsackievirus 2b protein g-coupled protein receptor voltage-dependent calcium channels steady-state [ca2+] levels isoform-specific ligand-binding affinity camp-dependent protein kinase cgmp-dependent protein kinase putative pore-forming domain acute b-cell leukemia g-protein coupled receptors mortalin/mthsp70/pbp74/grp75 ca2+-sensitive gfp constructs er-mitochondrial calcium communication long-term metabolic priming putative pore-forming region ca2+-sensitive mitochondrial dehydrogenases agonist-sensitive ca2+ stores 5-triphosphate-induced ca2+ release stimulus-dependent [ca2+] increases tumor-mediated lymphocyte apoptosis ca2+-induced membrane transition passive ca2+/2na+ exchanger tyrosine-kinase coupled receptors bidirectional ca2+-dependent control ca2+-dependent apoptotic stimuli akt hyper-activation induces store-operated calcium channels agonist-specific calcium signaling store-operated ca2+ channels endoplasmic reticulum-targeted bcl-2 er-resident ca2+ channels 5-trisphosphate-induced calcium release
Questions {❓}
- A mechanism for agonist-specific calcium signaling?
- Depressing ER/mitochondria Ca2+ crosstalk: an effective strategy for oncogenes?
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