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Regulation of breathing by CO2 requires the proton-activated receptor GPR4 in retrotrapezoid nucleus neurons
It is shown that selective expression of the proton-activated receptor GPR4 in chemosensory neurons of the mouse retrotrapezoid nucleus (RTN) is required for CO2-stimulated breathing, and the data identify G PR4 and TASK-2 as distinct, parallel, and essential central mediators of respiratory chemosensitivity.
S-Nitrosylation Inhibits Pannexin 1 Channel Function*
- A. Lohman, Janelle L Weaver, +8 authors B. Isakson
- Chemistry, MedicineThe Journal of Biological Chemistry
- 2 October 2012
The results provide the first evidence of a reversible post-translational modification on pannexin 1 to regulate channel activity and indicate that S-nitrosylation of Panx1 at Cys-40 and CYS-346 inhibits channel currents and ATP release.
Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane.
- B. M. Kenwood, Janelle L Weaver, +23 authors K. Hoehn
- Biology, MedicineMolecular metabolism
- 1 April 2014
BAM15 is bioactive in vivo and dose-dependently protects mice from acute renal ischemic-reperfusion injury and its reduced toxicity will hopefully reignite interest in pharmacological uncoupling for the treatment of the myriad of diseases that are associated with altered mitochondrial function.
Ion channel profile of TRPM8 cold receptors reveals a role of TASK-3 potassium channels in thermosensation.
A role of TASK-3 channels in thermosensation is demonstrated, showing that a channel-based combinatorial strategy in TRPM8 cold thermoreceptors leads to molecular specialization and functional diversity.
Hematopoietic pannexin 1 function is critical for neuropathic pain
- Janelle L Weaver, S. Arandjelovic, +12 authors D. Bayliss
- MedicineScientific reports
- 14 February 2017
It is shown that Pannexin 1 in hematopoietic cells is required for pain-like responses following nerve injury in mice, and inhibition of Panx1 may be useful in treating neuropathic pain, and a potential therapeutic target is suggested.
Nalcn Is a “Leak” Sodium Channel That Regulates Excitability of Brainstem Chemosensory Neurons and Breathing
- Yingtang Shi, Chikara Abe, +8 authors D. Bayliss
- Chemistry, MedicineThe Journal of Neuroscience
- 3 August 2016
It is shown that a leak Na+ channel, Nalcn, is expressed in the CO2/H+-sensitive neurons of the mouse retrotrapezoid nucleus (RTN) that regulate breathing, and a specific function for this enigmatic channel is defined in an important physiological context.
Channel Function -Nitrosylation Inhibits Pannexin 1 S Membrane Biology: