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Cellular calcium signalling and downstream consequences

Reference	BBS/E/B/0000C220
Principal Investigator / Supervisor	Dr Martin Bootman
Co-Investigators / Co-Supervisors
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	231,486
Status	Completed
Type	Institute Project
Start date	01/10/2004
End date	30/09/2007
Duration	36 months

Abstract

Calcium (Ca2+) is an almost universal cellular messenger, with physiological roles both inside and outside cells. Ca2+ signals are highly versatile- they can occur as brief events localised to specific regions within cells or traverse whole tissues in a regenerative manner. The enormous diversity of Ca2+ signals arises from the complex interplay of different mechanisms that serve to increase or decrease Ca2+ within cells. The types of response that a cell can display are a function of its `Ca2+ signalling proteome¿. Such proteomes are cell specific- no two cell types utilise exactly the same combinations of Ca2+ signalling systems and they therefore have unique responses. The Ca2+ concentration inside cells is finely regulated by the simultaneous interplay of multiple counteracting processes, which can be divided into Ca2+ `on¿ and `off¿ mechanisms depending on whether they serve to increase or decrease cytosolic Ca2+. The Ca2+ `on¿ mechanisms include channels located at the plasma membrane (PM) that regulate the supply of Ca2+ from the extracellular space, and channels on intracellular organelles such as the endoplasmic reticulum and sarcoplasmic reticulum (ER/SR) that release stored Ca2+. An equally diverse set of `off¿ mechanisms is employed by cells to remove Ca2+ from the cytoplasm. These include Ca2+ATPases on the PM and ER/SR, in addition to exchangers that utilise electrochemical gradients of other ions to provide the energy to transport Ca2+ out of the cell. Organelles other than the ER and SR also play important roles in Ca2+ homeostasis by sequestering or releasing Ca2+. For example, mitochondria have been shown to limit the amplitude of cytosolic Ca2+ increases by rapidly sequestering Ca2+, and then more slowly returning it to the cytoplasm. This project characterises Ca2+ signalling proteomes within specific cell types in order to understand how cells generate and interpret their unique Ca2+ signals.

Summary

unavailable

Committee	Closed Committee - Biochemistry & Cell Biology (BCB)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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