Modelling receptor-controlled intracellular calcium oscillators

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Modelling receptor-controlled intracellular calcium oscillators
Συγγραφείς: K S R Cuthbertson, T.R. Chay
Πηγή: Cell Calcium. 12:97-109
Στοιχεία εκδότη: Elsevier BV, 1991.
Έτος έκδοσης: 1991
Θεματικοί όροι: Enzyme Activation, Periodicity, GTP-Binding Proteins, Animals, Calcium, Receptors, Cell Surface, Models, Biological, Mathematics, Protein Kinase C
Περιγραφή: This paper presents mathematical models for the hepatocyte calcium oscillator which follow the concepts in a class of informal models developed to account for the striking dependence on the receptor type of several features of the calcium oscillations, in particular the shape and duration of the free calcium transients. The essence of these models is that the transients should be timed by a build-up of activated GTP-binding proteins, which, combined with positive feedback processes and perhaps with cooperative effects, leads to a sudden activation of phospholipase C (PLC), followed by negative feedback processes which switch off the calcium rise and lead to a fall in free calcium back to resting levels. These models predict pulsatile oscillations in inositol (1,4,5)P3 as well as in free calcium. We show that receptor-controlled intracellular calcium oscillators involving an unknown positive feedback pathway onto PLC and negative feedback from protein kinase C (PKC) onto G-proteins and receptors, or negative feedback by stimulation of GTPase activity can simulate many of the features of observed intracellular calcium oscillations. These oscillators exhibit a dependence of frequency on agonist concentration and a dependence of transient duration on receptor and G-protein type. We also show that a PLC-dependent GTPase activating factor (GAF) could provide explanations for some otherwise puzzling features of intracellular calcium oscillations.
Τύπος εγγράφου: Article
Γλώσσα: English
ISSN: 0143-4160
DOI: 10.1016/0143-4160(91)90012-4
Σύνδεσμος πρόσβασης: https://pubmed.ncbi.nlm.nih.gov/1647879
https://www.sciencedirect.com/science/article/abs/pii/0143416091900124
https://www.ncbi.nlm.nih.gov/pubmed/1647879
Rights: Elsevier TDM
Αριθμός Καταχώρησης: edsair.doi.dedup.....54a1100b8489d6966aac16da0f8044eb
Βάση Δεδομένων: OpenAIRE
Περιγραφή
ISSN:01434160
DOI:10.1016/0143-4160(91)90012-4