Role of STIM1 in the surface expression of SARAF

Albarrán, Letizia; Regodón, S.; Salido, Ginés M.; López, José J.; Rosado, Juan A.

doi:10.1080/19336950.2016.1212141

Cited by 20 publications

(13 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous study showed that SARAF negatively modulated SOCE by preventing the spontaneous activation of STIM1 and inhibiting the formation of the STIM1-Orai1 complex Cellular Physiology and Biochemistry [17,25]. The interaction between SARAF and STIM1-Orai1 was not fully understood; and it is still unknown how SARAF affects the expression of STIM1 and Orai1.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Overexpression of SARAF Ameliorates Pressure Overload–Induced Cardiac Hypertrophy Through Suppressing STIM1-Orai1 in Mice

Zhang

Wang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Activation of stromal interaction molecule 1 (STIM1) and Orai1 participates in the development of cardiac hypertrophy. Store-operated Ca²⁺ entry-associated regulatory factor (SARAF) is an intrinsic inhibitor of STIM1-Orai1 interaction. Thus, we hypothesized that SARAF could prevent cardiac hypertrophy. Methods: Male C57BL/6 mice, aged 8 weeks, were randomly divided into sham and abdominal aortic constriction surgery groups and were infected with lentiviruses expressing SARAF and GFP (Lenti-SARAF) or GFP alone (Lenti-GFP) via intramyocardial injection. At 4 weeks after aortic constriction, left ventricular structure and function were assessed by echocardiography and hemodynamic assays. The gene and protein expressions of SARAF, STIM1, and Orai1 were measured by quantitative PCR and Western blot, respectively. Results: Gene and protein expressions of SARAF were significantly decreased, while STIM1 and Orai1 were increased in the heart tissue compared with sham group. Overexpression of SARAF in the heart prevented the upregulation of STIM1 and Orai1, and importantly, attenuated aortic constriction-induced decrease in maximal rate of left ventricular pressure decay and increases in thickness of interventricular septum and left ventricular posterior wall, heart weight/body weight ratio, and size of cardiomyocytes. Blood pressure detected through the carotid artery and left ventricular systolic function were not affected by SARAF overexpression. In addition, overexpression of SARAF also attenuated angiotensin II-induced upregulation of STIM1 and Orai1 and hypertrophy of cultured cardiomyocytes. Conclusion: Overexpression of SARAF in the heart prevents cardiac hypertrophy, probably through suppressing the upregulation of STIM1/Orai1.

show abstract

Section: Discussionmentioning

confidence: 99%

“…SARAF likely interacts with Orail's C-terminal in a STIM1-independent manner [16]. It has also been reported that STIM1 can, in turn, affect the translocation of SARAF from ER to plasma membrane [25].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of SARAF Ameliorates Pressure Overload–Induced Cardiac Hypertrophy Through Suppressing STIM1-Orai1 in Mice

Zhang

Wang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Many proteins regulate SOCE, including α-SNAP, CRACR2A, golli, ORMDL3, SARAF, septins, STIMATE, and TMEM110 [ 31 – 42 ]. In addition to direct modulation of SOCE by its key players, other regulatory mechanisms can influence SOCE.…”

Section: Introductionmentioning

confidence: 99%

Store-Operated Ca2+ Entry as a Prostate Cancer Biomarker — a Riddle with Perspectives

et al. 2017

View full text Add to dashboard Cite

Purpose of ReviewStore-operated calcium entry (SOCE) is dysregulated in prostate cancer, contributing to increased cellular migration and proliferation and preventing cancer cell apoptosis. We here summarize findings on gene expression levels and functions of SOCE components, stromal interaction molecules (STIM1 and STIM2), and members of the Orai protein family (Orai1, 2, and 3) in prostate cancer. Moreover, we introduce new research models that promise to provide insights into whether dysregulated SOCE signaling has clinically relevant implications in terms of increasing the migration and invasion of prostate cancer cells.Recent FindingsRecent reports on Orai1 and Orai3 expression levels and function were in part controversial probably due to the heterogeneous nature of prostate cancer. Lately, in prostate cancer cells, transient receptor melastatin 4 channel was shown to alter SOCE and play a role in migration and proliferation. We specifically highlight new cancer research models: a subpopulation of cells that show tumor initiation and metastatic potential in mice and zebrafish models.SummaryThis review focuses on SOCE component dysregulation in prostate cancer and analyzes several preclinical, cellular, and animal cancer research models.

show abstract

“…Initially identified by Palty and colleagues, SARAF has been shown to be critical for slow Ca 2+ -dependent inactivation of CRAC channels [ 124 ] ( Figure 2 ). SARAF, later also identified to be eventually expressed in the plasma membrane in a manner dictated by surface-localized STIM1, engages dynamic interactions with STIM1 upon rest and in the course of activation, in addition to store-depletion dependent direct couplings to Orai1 [ 125 , 126 ]. (For review, see Jardín et al 2018 [ 127 ].)…”

Section: Regulators Of Crac Channel Functionmentioning

confidence: 99%

More Than Just Simple Interaction between STIM and Orai Proteins: CRAC Channel Function Enabled by a Network of Interactions with Regulatory Proteins

Berlansky

Humer

Sallinger

et al. 2021

IJMS

View full text Add to dashboard Cite

The calcium-release-activated calcium (CRAC) channel, activated by the release of Ca2+ from the endoplasmic reticulum (ER), is critical for Ca2+ homeostasis and active signal transduction in a plethora of cell types. Spurred by the long-sought decryption of the molecular nature of the CRAC channel, considerable scientific effort has been devoted to gaining insights into functional and structural mechanisms underlying this signalling cascade. Key players in CRAC channel function are the Stromal interaction molecule 1 (STIM1) and Orai1. STIM1 proteins span through the membrane of the ER, are competent in sensing luminal Ca2+ concentration, and in turn, are responsible for relaying the signal of Ca2+ store-depletion to pore-forming Orai1 proteins in the plasma membrane. A direct interaction of STIM1 and Orai1 allows for the re-entry of Ca2+ from the extracellular space. Although much is already known about the structure, function, and interaction of STIM1 and Orai1, there is growing evidence that CRAC under physiological conditions is dependent on additional proteins to function properly. Several auxiliary proteins have been shown to regulate CRAC channel activity by means of direct interactions with STIM1 and/or Orai1, promoting or hindering Ca2+ influx in a mechanistically diverse manner. Various proteins have also been identified to exert a modulatory role on the CRAC signalling cascade although inherently lacking an affinity for both STIM1 and Orai1. Apart from ubiquitously expressed representatives, a subset of such regulatory mechanisms seems to allow for a cell-type-specific control of CRAC channel function, considering the rather restricted expression patterns of the specific proteins. Given the high functional and clinical relevance of both generic and cell-type-specific interacting networks, the following review shall provide a comprehensive summary of regulators of the multilayered CRAC channel signalling cascade. It also includes proteins expressed in a narrow spectrum of cells and tissues that are often disregarded in other reviews of similar topics.

show abstract

Role of STIM1 in the surface expression of SARAF

Cited by 20 publications

References 14 publications

Overexpression of SARAF Ameliorates Pressure Overload–Induced Cardiac Hypertrophy Through Suppressing STIM1-Orai1 in Mice

Overexpression of SARAF Ameliorates Pressure Overload–Induced Cardiac Hypertrophy Through Suppressing STIM1-Orai1 in Mice

Store-Operated Ca2+ Entry as a Prostate Cancer Biomarker — a Riddle with Perspectives

More Than Just Simple Interaction between STIM and Orai Proteins: CRAC Channel Function Enabled by a Network of Interactions with Regulatory Proteins

Contact Info

Product

Resources

About