Regulation and role of store-operated ca2++ entry in cellular proliferation

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Citations (Scopus)

Abstract

Ca2++ is a ubiquitous intracellular messenger that transduces a variety of cellular responses downstream of the activation of G-protein-coupled or tyrosine kinase receptors. Depending on the agonist and cellular context, Ca2++ can mediate different responses in the same cell [1]. The specific cellular response transduced downstream of the particular Ca2++ transient is encoded in the spatial and temporal dynamics of the Ca2++ signal, leading to the activation of a subset of Ca2++-dependent effectors and the ensuing cellular response. As such, the duration, amplitude, frequency, and spatial localization of Ca2++ signals encode targeted signals that activate Ca2++-sensitive effectors to define a particular cellular response. To generate and fine-tune those Ca2++ signals, cells use two main Ca2++ sources: entry of extracellular Ca2++ and Ca2++ release from intracellular stores. The primary intracellular Ca2++ store is the endoplasmic reticulum (ER), which can concentrate Ca2++ in the hundreds of µM range [2].

Original languageEnglish
Title of host publicationCalcium Entry Channels in Non-Excitable Cells
PublisherCRC Press
Pages215-239
Number of pages25
ISBN (Electronic)9781498752732
ISBN (Print)9781498752725
DOIs
Publication statusPublished - 1 Jan 2017

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Chemical activation
Cell Proliferation
Receptor Protein-Tyrosine Kinases
GTP-Binding Proteins
Endoplasmic Reticulum

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Regulation and role of store-operated ca2++ entry in cellular proliferation. / Hodeify, Rawad; Yu, Fang; Courjaret, Raphael Jean; Nader, Nancy; Dib, Maya; Sun, Lu; Adap, Ethel; Hubrack, Satanay Zuhair; Machaca, Khaled.

Calcium Entry Channels in Non-Excitable Cells. CRC Press, 2017. p. 215-239.

Research output: Chapter in Book/Report/Conference proceedingChapter

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AU - Adap, Ethel

AU - Hubrack, Satanay Zuhair

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