OptoSTIM1

The review scaffold groups STIM1 optogenetic tools into at least CRY2-based oligomerization designs and LOV2-based unfolding or caging designs for optical control of calcium signaling.

The review scaffold explicitly names OptoSTIM1, monSTIM1, eOS1, Opto-CRAC1, Opto-CRAC2, BACCS, and LOVS1K as STIM1-related optogenetic calcium-control tools or variants within the review scope.

The review covers optogenetic tools for precise control of Ca2+-permeable ion channels, receptors, and associated downstream signaling cascades.

Here, we review the various optogenetic tools that have been used to achieve precise control over different Ca2+-permeable ion channels and receptors and associated downstream signaling cascades.

OptoCRAC tools enable remote and precise control of calcium signaling with high spatial and temporal resolution.

our single-component OptoCRAC tools provide new opportunities to remotely and precisely control the Ca^2+ signaling at high spatial and temporal resolution

OptoCRAC tools enable remote and precise control of calcium signaling with high spatial and temporal resolution.

our single-component OptoCRAC tools provide new opportunities to remotely and precisely control the Ca^2+ signaling at high spatial and temporal resolution

OptoCRAC tools enable remote and precise control of calcium signaling with high spatial and temporal resolution.

our single-component OptoCRAC tools provide new opportunities to remotely and precisely control the Ca^2+ signaling at high spatial and temporal resolution

OptoCRAC tools enable remote and precise control of calcium signaling with high spatial and temporal resolution.

our single-component OptoCRAC tools provide new opportunities to remotely and precisely control the Ca^2+ signaling at high spatial and temporal resolution

OptoCRAC tools enable remote and precise control of calcium signaling with high spatial and temporal resolution.

our single-component OptoCRAC tools provide new opportunities to remotely and precisely control the Ca^2+ signaling at high spatial and temporal resolution

OptoCRAC tools enable remote and precise control of calcium signaling with high spatial and temporal resolution.

our single-component OptoCRAC tools provide new opportunities to remotely and precisely control the Ca^2+ signaling at high spatial and temporal resolution

OptoCRAC tools enable remote and precise control of calcium signaling with high spatial and temporal resolution.

our single-component OptoCRAC tools provide new opportunities to remotely and precisely control the Ca^2+ signaling at high spatial and temporal resolution

OptoCRAC was successfully used to photo-tune Ca2+/NFAT-dependent gene expression and to reprogram endogenous gene transcription when coupled with CRISPR/Cas9.

We have successfully demonstrated the use of OptoCRAC to photo-tune Ca^2+/NFAT-dependent gene expression, as well as transcriptional reprogramming of endogenous genes when coupled with the CRISPR/Cas9 genome editing technique.

OptoCRAC was successfully used to photo-tune Ca2+/NFAT-dependent gene expression and to reprogram endogenous gene transcription when coupled with CRISPR/Cas9.

We have successfully demonstrated the use of OptoCRAC to photo-tune Ca^2+/NFAT-dependent gene expression, as well as transcriptional reprogramming of endogenous genes when coupled with the CRISPR/Cas9 genome editing technique.

OptoCRAC was successfully used to photo-tune Ca2+/NFAT-dependent gene expression and to reprogram endogenous gene transcription when coupled with CRISPR/Cas9.

We have successfully demonstrated the use of OptoCRAC to photo-tune Ca^2+/NFAT-dependent gene expression, as well as transcriptional reprogramming of endogenous genes when coupled with the CRISPR/Cas9 genome editing technique.

OptoCRAC was successfully used to photo-tune Ca2+/NFAT-dependent gene expression and to reprogram endogenous gene transcription when coupled with CRISPR/Cas9.

We have successfully demonstrated the use of OptoCRAC to photo-tune Ca^2+/NFAT-dependent gene expression, as well as transcriptional reprogramming of endogenous genes when coupled with the CRISPR/Cas9 genome editing technique.

OptoCRAC was successfully used to photo-tune Ca2+/NFAT-dependent gene expression and to reprogram endogenous gene transcription when coupled with CRISPR/Cas9.

We have successfully demonstrated the use of OptoCRAC to photo-tune Ca^2+/NFAT-dependent gene expression, as well as transcriptional reprogramming of endogenous genes when coupled with the CRISPR/Cas9 genome editing technique.

OptoCRAC was successfully used to photo-tune Ca2+/NFAT-dependent gene expression and to reprogram endogenous gene transcription when coupled with CRISPR/Cas9.

We have successfully demonstrated the use of OptoCRAC to photo-tune Ca^2+/NFAT-dependent gene expression, as well as transcriptional reprogramming of endogenous genes when coupled with the CRISPR/Cas9 genome editing technique.

OptoCRAC was successfully used to photo-tune Ca2+/NFAT-dependent gene expression and to reprogram endogenous gene transcription when coupled with CRISPR/Cas9.

We have successfully demonstrated the use of OptoCRAC to photo-tune Ca^2+/NFAT-dependent gene expression, as well as transcriptional reprogramming of endogenous genes when coupled with the CRISPR/Cas9 genome editing technique.

cpLOV2 variants were developed through circular permutation to create new interfaces for caging protein function.

we developed a series of engineered LOV2 variants (cpLOV2) through circular permutation. cpLOV2 creates new interfaces to cage protein function

OptoORAI1 was generated by inserting LOV2 into the loop region of ORAI1 so that LOV2 acts as an allosteric switch to open the channel.

To generate OptoORAI1, LOV2 was inserted into the loop region of ORAI1 and thus acted as an allosteric switch to induce structural rearrangement within ORAI1 to open the channel.

OptoORAI1 was generated by inserting LOV2 into the loop region of ORAI1 so that LOV2 acts as an allosteric switch to open the channel.

To generate OptoORAI1, LOV2 was inserted into the loop region of ORAI1 and thus acted as an allosteric switch to induce structural rearrangement within ORAI1 to open the channel.

OptoORAI1 was generated by inserting LOV2 into the loop region of ORAI1 so that LOV2 acts as an allosteric switch to open the channel.

To generate OptoORAI1, LOV2 was inserted into the loop region of ORAI1 and thus acted as an allosteric switch to induce structural rearrangement within ORAI1 to open the channel.

OptoORAI1 was generated by inserting LOV2 into the loop region of ORAI1 so that LOV2 acts as an allosteric switch to open the channel.

To generate OptoORAI1, LOV2 was inserted into the loop region of ORAI1 and thus acted as an allosteric switch to induce structural rearrangement within ORAI1 to open the channel.

OptoORAI1 was generated by inserting LOV2 into the loop region of ORAI1 so that LOV2 acts as an allosteric switch to open the channel.

To generate OptoORAI1, LOV2 was inserted into the loop region of ORAI1 and thus acted as an allosteric switch to induce structural rearrangement within ORAI1 to open the channel.

OptoORAI1 was generated by inserting LOV2 into the loop region of ORAI1 so that LOV2 acts as an allosteric switch to open the channel.

To generate OptoORAI1, LOV2 was inserted into the loop region of ORAI1 and thus acted as an allosteric switch to induce structural rearrangement within ORAI1 to open the channel.

OptoORAI1 was generated by inserting LOV2 into the loop region of ORAI1 so that LOV2 acts as an allosteric switch to open the channel.

To generate OptoORAI1, LOV2 was inserted into the loop region of ORAI1 and thus acted as an allosteric switch to induce structural rearrangement within ORAI1 to open the channel.

OptoSTIM1 was engineered by combining the STIM1 SOAR region with the LOV2 domain.

OptoSTIM1 was engineered by combining STIM1-ORAI1 activation region (SOAR) of STIM1 with the light-reactive light-oxygen-voltage (LOV2) domain.

OptoSTIM1 was engineered by combining the STIM1 SOAR region with the LOV2 domain.

OptoSTIM1 was engineered by combining STIM1-ORAI1 activation region (SOAR) of STIM1 with the light-reactive light-oxygen-voltage (LOV2) domain.

OptoSTIM1 was engineered by combining the STIM1 SOAR region with the LOV2 domain.

OptoSTIM1 was engineered by combining STIM1-ORAI1 activation region (SOAR) of STIM1 with the light-reactive light-oxygen-voltage (LOV2) domain.

OptoSTIM1 was engineered by combining the STIM1 SOAR region with the LOV2 domain.

OptoSTIM1 was engineered by combining STIM1-ORAI1 activation region (SOAR) of STIM1 with the light-reactive light-oxygen-voltage (LOV2) domain.

OptoSTIM1 was engineered by combining the STIM1 SOAR region with the LOV2 domain.

OptoSTIM1 was engineered by combining STIM1-ORAI1 activation region (SOAR) of STIM1 with the light-reactive light-oxygen-voltage (LOV2) domain.

OptoSTIM1 was engineered by combining the STIM1 SOAR region with the LOV2 domain.

OptoSTIM1 was engineered by combining STIM1-ORAI1 activation region (SOAR) of STIM1 with the light-reactive light-oxygen-voltage (LOV2) domain.

OptoSTIM1 was engineered by combining the STIM1 SOAR region with the LOV2 domain.

OptoSTIM1 was engineered by combining STIM1-ORAI1 activation region (SOAR) of STIM1 with the light-reactive light-oxygen-voltage (LOV2) domain.

Randomized screening and optimization identified an OptoORAI1 variant with high light-induced calcium response change and no noticeable dark activity.

Through several rounds of randomized screening and optimization, we identified one OptoORAI1 variant exhibiting a high dynamic change in the light-induced Ca^2+ response without noticeable dark activity.

Randomized screening and optimization identified an OptoORAI1 variant with high light-induced calcium response change and no noticeable dark activity.

Through several rounds of randomized screening and optimization, we identified one OptoORAI1 variant exhibiting a high dynamic change in the light-induced Ca^2+ response without noticeable dark activity.

Randomized screening and optimization identified an OptoORAI1 variant with high light-induced calcium response change and no noticeable dark activity.

Through several rounds of randomized screening and optimization, we identified one OptoORAI1 variant exhibiting a high dynamic change in the light-induced Ca^2+ response without noticeable dark activity.

Randomized screening and optimization identified an OptoORAI1 variant with high light-induced calcium response change and no noticeable dark activity.

Through several rounds of randomized screening and optimization, we identified one OptoORAI1 variant exhibiting a high dynamic change in the light-induced Ca^2+ response without noticeable dark activity.

Randomized screening and optimization identified an OptoORAI1 variant with high light-induced calcium response change and no noticeable dark activity.

Through several rounds of randomized screening and optimization, we identified one OptoORAI1 variant exhibiting a high dynamic change in the light-induced Ca^2+ response without noticeable dark activity.

Randomized screening and optimization identified an OptoORAI1 variant with high light-induced calcium response change and no noticeable dark activity.

Through several rounds of randomized screening and optimization, we identified one OptoORAI1 variant exhibiting a high dynamic change in the light-induced Ca^2+ response without noticeable dark activity.

Randomized screening and optimization identified an OptoORAI1 variant with high light-induced calcium response change and no noticeable dark activity.

Through several rounds of randomized screening and optimization, we identified one OptoORAI1 variant exhibiting a high dynamic change in the light-induced Ca^2+ response without noticeable dark activity.

This review covers an optogenetic toolkit for precise control of calcium signaling, including genetically encoded calcium actuators and multiple mechanistic classes such as STIM1/CRAC-based, GPCR-based, RTK-based, and channel-based approaches.

Melanopsin and Opto-XRs are discussed in the review as GPCR-based optogenetic routes relevant to calcium signaling control.

Opto-RTKs are discussed in the review as receptor-tyrosine-kinase-based optogenetic tools within the calcium-control toolkit.

OptoSTIM1 and Opto-CRAC are discussed in the review as STIM1/CRAC-based optogenetic tools for controlling calcium signaling.

PACR is discussed in the review as a genetically encoded photoactivatable calcium releaser for optical control of calcium signaling.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

The review scaffold groups STIM1 optogenetic tools into at least CRY2-based oligomerization designs and LOV2-based unfolding or caging designs for optical control of calcium signaling.

Source: Adaptation of STIM1 structure-function relationships for optogenetic control of calcium signaling

The review scaffold explicitly names OptoSTIM1, monSTIM1, eOS1, Opto-CRAC1, Opto-CRAC2, BACCS, and LOVS1K as STIM1-related optogenetic calcium-control tools or variants within the review scope.

Source: Adaptation of STIM1 structure-function relationships for optogenetic control of calcium signaling

The review covers optogenetic tools for precise control of Ca2+-permeable ion channels, receptors, and associated downstream signaling cascades.

Here, we review the various optogenetic tools that have been used to achieve precise control over different Ca2+-permeable ion channels and receptors and associated downstream signaling cascades.

Source: Deciphering Molecular Mechanisms and Intervening in Physiological and Pathophysiological Processes of Ca2+ Signaling Mechanisms Using Optogenetic Tools

OptoSTIM1 was engineered by combining the STIM1 SOAR region with the LOV2 domain.

OptoSTIM1 was engineered by combining STIM1-ORAI1 activation region (SOAR) of STIM1 with the light-reactive light-oxygen-voltage (LOV2) domain.

Source: Engineered CRAC Channel for Optical Control of Calcium Signaling

This review covers an optogenetic toolkit for precise control of calcium signaling, including genetically encoded calcium actuators and multiple mechanistic classes such as STIM1/CRAC-based, GPCR-based, RTK-based, and channel-based approaches.

Source: Optogenetic toolkit for precise control of calcium signaling

OptoSTIM1 and Opto-CRAC are discussed in the review as STIM1/CRAC-based optogenetic tools for controlling calcium signaling.

Source: Optogenetic toolkit for precise control of calcium signaling

OptoSTIM1 enabled quantitative and qualitative control of intracellular Ca2+ levels in various biological systems including zebrafish embryos and human embryonic stem cells.

We quantitatively and qualitatively controlled intracellular Ca(2+) levels in various biological systems, including zebrafish embryos and human embryonic stem cells.

Source: Optogenetic control of endogenous Ca2+ channels in vivo

Activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation.

Source: Optogenetic control of endogenous Ca2+ channels in vivo

OptoSTIM1 combines a plant photoreceptor and the CRAC channel regulator STIM1.

Using OptoSTIM1, which combines a plant photoreceptor and the CRAC channel regulator STIM1...

Source: Optogenetic control of endogenous Ca2+ channels in vivo

OptoSTIM1 is proposed to expand mechanistic understanding of Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.

The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca(2+)-associated processes and facilitate screening for drug candidates that antagonize Ca(2+) signals.

Source: Optogenetic control of endogenous Ca2+ channels in vivo

OptoSTIM1 is an optogenetic tool for manipulating intracellular Ca2+ levels through activation of endogenous CRAC channels.

Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca(2+) levels through activation of Ca(2+)-selective endogenous Ca(2+) release-activated Ca(2+) (CRAC) channels.

Source: Optogenetic control of endogenous Ca2+ channels in vivo