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Calcium Signalling
| Question | Answer |
|---|---|
| Allbritton et al 1992 | IP3 is a better global messenger than calcium as calcium is slowed by its binding to multiple proteins and buffered by the same. IP3 has the capacity to travel larger distances faster |
| Berridge et al 2000 | Review of calcium entry, leads to further sources but these are unverified |
| Feske et al 2003 | Description of Orai1 as the channel responsible for SOC. Found by screening consangineous SCID patients with defects in SOC, also a genome-wide RNAi screen in drosophila to disrupt SOC. Addition of wt Orai to SCID T cells recovered SOC. |
| Lefkimmiatis et al 2009 | Lowered ER calcium using chelator and showed that ACs are recruited, increases cAMP (FRET indicators), activates PKA. STIM1 allows ER calcium to signal through cAMP as STIM1 knockdown reduced cAMP response. |
| Lewis 2012 (no other authors) | Review of store operated Ca (SOC) channels. Jim Putney proposed SOC 25 years ago. ER Ca must be 25% down before Ca release activated channels (CRAC) become a factor. Relocation of Stim1 + Orai takes up to 10 secs (muscle <1 sec, prelocalised Edwards 2010) |
| Marchant and Parker 2000 | Wave freq incr involves sensit of CICR (Ca induced Ca release). Puffs incr freq and amplitude until one triggers a wave, then refractory. Ca waves tend to arise from the same area (similar to axon hillock). A few puff sites caused vast majority of waves. |
| Rizzuto and Pozzan 2003 | Review: mutations of Ca signalling. MPTP opens earlier in Huntingtons mito (or any given a polyglu tract), less able to survive. RyR mutations = malignant hyperthermia. ER Ca interventions have been shown to improve F508 CFTR traffic, diff to replicate. |
| Rizzuto et al 2012 | Review: Mito in Ca signalling. Ca 1st seen signalling by Ringer 1883, saw it causing contraction of isolated hearts. Rizzuto 92 showed fast entry of Ca into mito, used aequorin w/ mito target seq. Mito local w/ IP3R and RyR to overcome low MCU affinity |
| Baughman et al 2011 | Found MCU. Searched for proteins whose expression was linked to that of a regulatory protein. Then tagged both and showed that immunoprec of one brought up the other. Injected siRNA to novel partner and showed physiological function of MCU was impaired. |
| Odermatt et al 1996 | Showed that Brody disease was caused by a defect in SERCA. Found inactivating and truncating mutations in both chromosomes, recessive. Knew where to look as SERCA had been suggested as a target then localised to a region of chromosome 16 prior to this |
| Tinel et al 1999 | Mito form a barrier around the secretion zone of pancreatic exocrine cells, uncoupling these mito with CCCP led to a mopre global signal. Mitofusins seem to hold them in place. Presence of mitochondria localises calcium cycling |
| Bano et al 2005 | Showed that plasma membrane NCX is cleaved by calpain in excitotoxicity, prevents cell from recovering. Overexpression of calpain inhibitor or uncleavable isoform prevented late irrecoverable Ca rise normally seen in excit-tox |
| Roberts 1994 (only author) | Active extrusion has little effect on calcium levels in the locality of a channel as the channel's capacity far outstrips the extrusion mechanisms |
| Rizzuto et al 2009 | Review of calcium movement from ER to mitochondria. Important phenomenon in cell death and signalling to incr ATP production |
Created by:
Jonmassie
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