IP3 receptors and Ca2+ entry

Thillaiappan, Nagendra Babu; Chakraborty, Pragnya; Hasan, Gaiti; Taylor, Colin W.

doi:10.1016/j.bbamcr.2018.11.007

Cited by 65 publications

(51 citation statements)

References 107 publications

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“…We suggest that licensed IP 3 Rs held alongside ER-PM junctions may be the basic functional units of SOCE, allowing IP 3 to cause a substantial loss of Ca 2+ from the ER that regulates SOCE without trespassing into the remaining ER ( Fig. 5E; Thillaiappan et al 2017Thillaiappan et al , 2019Taylor and Machaca 2019).…”

Section: Ip 3 Receptorsmentioning

confidence: 93%

“…We need also to consider whether the scaffolding of signaling proteins by IP 3 Rs serves only to funnel information toward an IP 3evoked Ca 2+ signal, or might these scaffolds fulfil additional, and possibly unrelated, roles. There is, for example, evidence that IP 3 Rs, independent of their ability to release Ca 2+ from the ER, can modulate SOCE (Chakraborty et al 2016) and, since the mechanisms are not yet clear (Thillaiappan et al 2019), they may arise through scaffolding of proteins by IP 3 Rs.…”

Section: Cite This Article Asmentioning

confidence: 99%

“…We focus on recent progress toward understanding the structural basis of IP 3 R activation, evidence that IP 3 Rs are regulated by many additional proteins, and the organization of IP 3 Rs within ER membranes and the implications of that for SOCE. Other reviews provide readers with broader overviews (Foskett et al 2007), historical perspectives (Berridge 2005;Rossi and Taylor 2019), and more focused considerations of IP 3 Rs and disease (Berridge 2016;Hisatsune and Mikoshiba 2017;Egorova and Bezprozvanny 2018), their regulation by proteolysis (Wang and Yule 2018) and other signals (Prole and Taylor 2016;Taylor 2017), the evolution of IP 3 Rs (Alzayady et al 2015), and relationships between SOCE and IP 3 Rs (Taylor and Machaca 2019;Thillaiappan et al 2019). We begin with a short overview of IP 3 Rs.…”

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confidence: 99%

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Structure and Function of IP₃Receptors

Prole

Taylor

2019

Cold Spring Harb Perspect Biol

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139

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Inositol 1,4,5-trisphosphate receptors (IP 3 Rs), by releasing Ca 2+ from the endoplasmic reticulum (ER) of animal cells, allow Ca 2+ to be redistributed from the ER to the cytosol or other organelles, and they initiate store-operated Ca 2+ entry (SOCE). For all three IP 3 R subtypes, binding of IP 3 primes them to bind Ca 2+ , which then triggers channel opening. We are now close to understanding the structural basis of IP 3 R activation. Ca 2+ -induced Ca 2+ release regulated by IP 3 allows IP 3 Rs to regeneratively propagate Ca 2+ signals. The smallest of these regenerative events is a Ca 2+ puff, which arises from the nearly simultaneous opening of a small cluster of IP 3 Rs. Ca 2+ puffs are the basic building blocks for all IP 3 -evoked Ca 2+ signals, but only some IP 3 clusters, namely those parked alongside the ER-plasma membrane junctions where SOCE occurs, are licensed to respond. The location of these licensed IP 3 Rs may allow them to selectively regulate SOCE.

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Section: Ip 3 Receptorsmentioning

confidence: 93%

Section: Cite This Article Asmentioning

confidence: 99%

mentioning

confidence: 99%

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Structure and Function of IP₃Receptors

Prole

Taylor

2019

Cold Spring Harb Perspect Biol

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139

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“…Activated STIM1 will then translocate into ER-PM junctions to bind with and activate Orai1, the pore forming subunit of CRAC channels, causing Ca 2+ influxes [18]. Thus the activation of IP 3 Rs and CRAC channels is spatiotemporally coupled around ER-PM junctions [22]. Even though Ca 2+ release signals generated by IP 3 Rs and Ca 2+ influxes through CRAC channels occur at different subcellular regions, mediating different cellular processes [23,24], IP 3 Rs and CRAC channels are functionally coupled [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Type 3 Inositol 1,4,5-Trisphosphate Receptor is a Crucial Regulator of Calcium Dynamics Mediated by Endoplasmic Reticulum in HEK Cells

Yue

Wang

et al. 2020

Cells

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Being the largest the Ca2+ store in mammalian cells, endoplasmic reticulum (ER)-mediated Ca2+ signalling often involves both Ca2+ release via inositol 1, 4, 5-trisphosphate receptors (IP3R) and store operated Ca2+ entries (SOCE) through Ca2+ release activated Ca2+ (CRAC) channels on plasma membrane (PM). IP3Rs are functionally coupled with CRAC channels and other Ca2+ handling proteins. However, it still remains less well defined as to whether IP3Rs could regulate ER-mediated Ca2+ signals independent of their Ca2+ releasing ability. To address this, we generated IP3Rs triple and double knockout human embryonic kidney (HEK) cell lines (IP3Rs-TKO, IP3Rs-DKO), and systemically examined ER Ca2+ dynamics and CRAC channel activity in these cells. The results showed that the rate of ER Ca2+ leakage and refilling, as well as SOCE were all significantly reduced in IP3Rs-TKO cells. And these TKO effects could be rescued by over-expression of IP3R3. Further, results showed that the diminished SOCE was caused by NEDD4L-mediated ubiquitination of Orai1 protein. Together, our findings indicate that IP3R3 is one crucial player in coordinating ER-mediated Ca2+ signalling.

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“…cGMP has a dual action on Ca 2+ entry in pancreatic acini, attributable to the Ca 2+ sensitivity of NOS with respect to cytosolic and store Ca 2+ (Xu et al 1994). IP3 receptors link with extracellular signals and the phospholipase C pathway to facilitate the rapid passage of Ca 2+ from endoplasmic reticulum to cytosol and stimulation of store-operated calcium entry (SOCE) (Thillaiappan et al 2019). cGMP/ PKG signaling regulates IP3R activity, promoting endoplasmic reticulum stress and apoptosis of cone photoreceptors in mice deficient in cyclic nucleotide-gated (CNG) channels (Ma et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Tumour initiation, store-operated calcium entry (SOCE) and apoptosis: cyclic nucleotide dependence

Williams

2020

gpb

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Chemical instigators and modulators of tumourigenesis influence cell signal transduction pathways. Cyclic nucleotides and steroid hormones may contribute to the process of carcinogenesis or provide protection via apoptotic mechanisms. Although several pharmacologic classes of compounds influence cyclic nucleotide levels markedly, less is known about the class effects of promoters and blockers of tumourigenesis and apoptosis. This molecular modeling study uses cyclic nucleotide templates to investigate relative molecular similarity within compounds modulating tumourigenesis and apoptosis. Findings, in respect of superimposition and molecular fit of the investigated compounds, are related to their individual effects on cyclic nucleotide pharmacology. Modulators of tumourigenesis and estrogen receptor sub-type ligands relate to cyclic nucleotide structure. Estradiol and GPER ligands provide a similar pattern of fit to adenine nucleotide. Chemically diverse modulators of apoptosis, including K + channel ligands, fit to different components of cyclic nucleotide structure. Compounds modulating Ca 2+ entry and IP3 receptors relate structurally to the nucleotide dioxaphosphinin moiety. Relative molecular similarity within the structures of apoptosis and tumourigenesis modulators identifies a unifying property within chemically disparate compounds. The ubiquitous generation of oxidative stress and ROS in cells by apoptosis modulating compounds may relate to the disruption of cyclic nucleotide regulated homeostasis mechanisms.

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IP3 receptors and Ca2+ entry

Cited by 65 publications

References 107 publications

Structure and Function of IP₃Receptors

Structure and Function of IP₃Receptors

Type 3 Inositol 1,4,5-Trisphosphate Receptor is a Crucial Regulator of Calcium Dynamics Mediated by Endoplasmic Reticulum in HEK Cells

Tumour initiation, store-operated calcium entry (SOCE) and apoptosis: cyclic nucleotide dependence

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IP3 receptors and Ca2+ entry

Cited by 65 publications

References 107 publications

Structure and Function of IP3Receptors

Structure and Function of IP3Receptors

Type 3 Inositol 1,4,5-Trisphosphate Receptor is a Crucial Regulator of Calcium Dynamics Mediated by Endoplasmic Reticulum in HEK Cells

Tumour initiation, store-operated calcium entry (SOCE) and apoptosis: cyclic nucleotide dependence

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Product

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Structure and Function of IP₃Receptors

Structure and Function of IP₃Receptors