CRAC channels and ca2+-dependent gene expression

Yi Chun Yeh, Anant B. Parekh

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

11 Scopus citations


In order to respond to changes in the environment, cells need to switch genes on and off. One conserved mechanism that links events at the cell surface to gene expression in the nucleus employs intracellular Ca2++. A cytoplasmic Ca2++ rise stimulates Ca2++- dependent transcription factors, which then regulate gene activity. In neurons, Ca2++ entry through voltage-gated Ca2++ channels activates Ca2++-calmodulin-dependent protein kinases, leading to the phosphorylation of the transcription factor CREB (cAMP response-element binding protein) [1,2]. Phosphorylated CREB is thought to be involved in long-term potentiation [3], a form of learning and memory in the nervous system. In immune cells, transcription factors such as c-fos and the nuclear factor of activated T cells (NFAT) are activated by Ca2++ influx through store-operated Ca2++- release-activated Ca2++ (CRAC) channels [4,5]. These transcription factors often work in tandem to control the expression of chemokines and cytokines that are involved in both the innate and adaptive immune responses [6]. NFAT proteins are a family of five cytosolic proteins that migrate into the nucleus upon activation. For four of the members, translocation is triggered by a rise in cytoplasmic Ca2++ concentration [5,7]. NFATs are extensively phosphorylated at rest, resulting in the masking of a nuclear.

Original languageEnglish
Title of host publicationCalcium Entry Channels in Non-Excitable Cells
PublisherCRC Press
Number of pages13
ISBN (Electronic)9781498752732
ISBN (Print)9781498752725
StatePublished - 01 01 2017
Externally publishedYes

Bibliographical note

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© 2017 by Taylor & Francis Group, LLC.


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