ArticlePflugers Archiv : European journal of physiology2015
Dexamethasone activates transient receptor potential canonical 4 (TRPC4) channels via Rasd1 small GTPase pathway.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Role of transient receptor potential channels on pathogenesis and treatment of psoriasis.Inflammopharmacology · 2026Review
- Unique responses of the fixed stoichiometric TRPC1-TRPC5 concatemer to G proteins.Frontiers in physiology · 2024Article
- Expression of Rasd1 in mouse endocrine pituitary cells and its response to dexamethasone.Stress (Amsterdam, Netherlands) · 2021Article
- Review
- The regulation of transient receptor potential canonical 4 (TRPC4) channel by phosphodiesterase 5 inhibitor via the cyclic guanosine 3'5'-monophosphate.Pflugers Archiv : European journal of physiology · 2017Article
- Rasd1, a small G protein with a big role in the hypothalamic response to neuronal activation.Molecular brain · 2016Article
- The Roles of Rasd1 small G proteins and leptin in the activation of TRPC4 transient receptor potential channels.Channels (Austin, Tex.) · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Canonical transient receptor potential 4 (TRPC4) channels are calcium-permeable, nonselective cation channels that are widely distributed in mammalian cells. It is generally speculated that TRPC4 channels are activated by Gq/11-PLC pathway or directly activated by Gi/o proteins. Although many mechanistic studies regarding TRPC4 have dealt with heterotrimeric G proteins, here, we first report the functional relationship between TRPC4 and small GTPase, Rasd1. Rasd1 selectively activated TRPC4 channels, and it was the only Ras protein among Ras protein family that can activate TRPC4 channels. For this to occur, it was found that certain population of functional Gαi1 and Gαi3 proteins are essential. Meanwhile, dexamethasone, a synthetic glucocorticoid and anti-inflammatory drug was known to increase messenger RNA (mRNA) level of Rasd1 in pancreatic β-cells. We have found that dexamethasone triggers TRPC4-like cationic current in INS-1 cells via increasing protein expression level of Rasd1. This relationship among dexamethasone, Rasd1, and TRPC4 could suggest a new therapeutic agent for hospitalized diabetes mellitus (DM) patients with prolonged dexamethasone prescription.
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Registered trials
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