Skip to main content

T-type Ca 2+ channel blocker mibefradil blocks ORAI channels via acting on extracellular surface (2019)
Journal Article
Li, P., Rubaiy, H. N., Chen, G., Hallett, T., Zaibi, N., Zeng, B., …Xu, S. (in press). T-type Ca 2+ channel blocker mibefradil blocks ORAI channels via acting on extracellular surface. British Journal of Pharmacology, https://doi.org/10.1111/bph.14788

Background and purpose Mibefradil (Mib), a T‐type Ca2+ channel blocker, has been investigated for treating solid tumours. However, its underlying mechanisms are still unclear. Here we aimed to investigate the pharmacological aspect of Mib on ORAI st... Read More about T-type Ca 2+ channel blocker mibefradil blocks ORAI channels via acting on extracellular surface.

ORAI channels are critical for receptor-mediated endocytosis of albumin (2017)
Journal Article
Zeng, B., Chen, G., Garcia-Vaz, E., Bhandari, S., Daskoulidou, N., Berglund, L. M., …Xu, S. (2017). ORAI channels are critical for receptor-mediated endocytosis of albumin. Nature communications, 8(1), https://doi.org/10.1038/s41467-017-02094-y

Impaired albumin reabsorption by proximal tubular epithelial cells (PTECs) has been highlighted in diabetic nephropathy (DN), but little is known about the underlying molecular mechanisms. Here we find that ORAI1-3, are preferentially expressed in PT... Read More about ORAI channels are critical for receptor-mediated endocytosis of albumin.

High glucose enhances store-operated calcium entry by upregulating ORAI/STIM via calcineurin-NFAT signalling (2014)
Journal Article
Daskoulidou, N., Xu, S. Z., Zeng, B., Gomez, M. F., Berglund, L. M., Atkin, S. L., …Daskoulidou, N. (2015). High glucose enhances store-operated calcium entry by upregulating ORAI/STIM via calcineurin-NFAT signalling. Journal of Molecular Medicine, 93(5), 511-521. https://doi.org/10.1007/s00109-014-1234-2

© 2014, Springer-Verlag Berlin Heidelberg. Abstract: ORAI and stromal interaction molecule (STIM) are store-operated channel molecules that play essential roles in human physiology through a coupling mechanism of internal Ca 2+ store to Ca 2+ influx.... Read More about High glucose enhances store-operated calcium entry by upregulating ORAI/STIM via calcineurin-NFAT signalling.

The ryanodine receptor agonist 4-chloro-3-ethylphenol blocks ORAI store-operated channels: 4-Chloro-3-ethylphenol inhibits ORAI channels (2014)
Journal Article
Zeng, B., Chen, G., Daskoulidou, N., & Xu, S. (2014). The ryanodine receptor agonist 4-chloro-3-ethylphenol blocks ORAI store-operated channels: 4-Chloro-3-ethylphenol inhibits ORAI channels. British Journal of Pharmacology, 171(5), 1250-1259. https://doi.org/10.1111/bph.12528

Background Depletion of the Ca2+ store by ryanodine receptor (RyR) agonists induces store‐operated Ca2+ entry (SOCE). 4‐Chloro‐3‐ethylphenol (4‐CEP) and 4‐chloro‐m‐cresol (4‐CmC) are RyR agonists commonly used as research tools and diagnostic reagen... Read More about The ryanodine receptor agonist 4-chloro-3-ethylphenol blocks ORAI store-operated channels: 4-Chloro-3-ethylphenol inhibits ORAI channels.

Store-independent pathways for cytosolic STIM1 clustering in the regulation of store-operated Ca2+ influx (2012)
Journal Article
Zeng, B., Chen, G., & Xu, S. Z. (2012). Store-independent pathways for cytosolic STIM1 clustering in the regulation of store-operated Ca2+ influx. Biochemical Pharmacology, 84(8), (1024-1035). doi:10.1016/j.bcp.2012.07.013. ISSN 1873-2968

STIM1 is a Ca 2+ sensing molecule. Once the Ca 2+ stores are depleted, STIM1 moves towards the plasma membrane (PM) (translocation), forms puncta (clustering), and triggers store-operated Ca 2+ entry (SOCE). Although this process has been regarded as... Read More about Store-independent pathways for cytosolic STIM1 clustering in the regulation of store-operated Ca2+ influx.

Pharmacological comparison of novel synthetic fenamate analogues with econazole and 2-APB on the inhibition of TRPM2 channels (2012)
Journal Article
Chen, G., Zeng, B., Eastmond, S., Elsenussi, S. E., Boa, A. N., & Xu, S. (2012). Pharmacological comparison of novel synthetic fenamate analogues with econazole and 2-APB on the inhibition of TRPM2 channels. British Journal of Pharmacology, 167(6), 1232-1243. https://doi.org/10.1111/j.1476-5381.2012.02058.x

BACKGROUND: Fenamate analogues, econazole and 2-APB are inhibitors of TRPM2 channels, which have been used as research tools. However, these compounds have different chemical structures and therapeutic applications. Here we aimed to investigate the p... Read More about Pharmacological comparison of novel synthetic fenamate analogues with econazole and 2-APB on the inhibition of TRPM2 channels.

Effect of non-steroidal anti-inflammatory drugs and new fenamate analogues on TRPC4 and TRPC5 channels (2012)
Journal Article
Xu, S., Boa, A., Atkin, S., Elsenussi, S., Chen, G., Bot, D., …Xu, S. Z. (2012). Effect of non-steroidal anti-inflammatory drugs and new fenamate analogues on TRPC4 and TRPC5 channels. Biochemical Pharmacology, 83(7), 923-931. https://doi.org/10.1016/j.bcp.2012.01.014

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used anti-inflammatory therapeutic agents,among which the fenamate analogues play important roles in regulating intracellular Ca2+ transient and ion channels. However, the effect of NSAIDs on... Read More about Effect of non-steroidal anti-inflammatory drugs and new fenamate analogues on TRPC4 and TRPC5 channels.

Activation of TRPC cationic channels by mercurial compounds confers the cytotoxicity of mercury exposure (2011)
Journal Article
Xu, S., Zeng, B., Atkin, S. L., Daskoulidou, N., Chen, G., & Lukhele, B. (2012). Activation of TRPC cationic channels by mercurial compounds confers the cytotoxicity of mercury exposure. Toxicological Sciences, 125(1), 56 - 68. https://doi.org/10.1093/toxsci/kfr268

Mercury is an established worldwide environmental pollutant with well-known toxicity affecting neurodevelopment in humans, but the molecular basis of cytotoxicity and the detoxification procedure are still unclear. Here we examined the involvement of... Read More about Activation of TRPC cationic channels by mercurial compounds confers the cytotoxicity of mercury exposure.


;