Special Issue "Ca2+-Activated Chloride Channels and Phospholipid Scramblases"
Deadline for manuscript submissions: 31 March 2021.
Interests: ion channels; scramblases; membrane biophysics; electrophysiology; Ca-activated chloride channels; TMEM16; volume-regulated chloride channels; molecular and cellular mechanisms of genetic diseases; olfaction; olfactory transduction; channelopathies; intracellular channels
Interests: ion channels; scramblases; membrane biophysics; electrophysiology; Ca-activated chloride channels; TMEM16; olfaction; olfactory transduction; vomeronsal trasnduction
TMEM16A/Ano1 and TMEM16B/Ano2 form Ca2+-activated Cl– channels that are involved in a variety of physiological functions, such as transepithelial ion transport, olfaction, phototransduction, smooth muscle contraction, nociception, cell proliferation and neuronal excitability.
Ca2+-activated Cl– currents were first observed in the early 1980s in the salamander retina and in Xenopus laevis oocytes, however the lack of knowledge on their molecular identity and poor pharmacological tools has slowed the comprehension of their specific physiological functions for a long time. Additionally, a full comprehension of their function cannot neglect the equilibrium potential for chloride. In the central and peripheral nervous systems, a contribution of these currents to cellular excitability has been proposed, either excitatory, as in dorsal root ganglion neurons and olfactory sensory neurons, or inhibitory, as in thalamocortical neurons.
Surprisingly, despite sharing a similar structural organization, other members of the TMEM16/Anoctamin family have a completely different molecular function: these so-called Ca2+ dependent phospholipid scramblases mediate the passive transfer of phospholipids between the leaflets of the membrane bilayer, causing the regulated collapse of membrane asymmetry.
While the TMEM16F/Ano6 scramblase resides in the plasma membrane, others, including TMEM16E/Ano5 and TMEM16K/Ano10 may function in intracellular membranes. Mutations in several TMEM16/Anoctamin genes, TMEM16C/Ano3, TMEM16E/Ano5, TMEM16F/Ano6 and TMEM16K/Ano10, cause various genetic diseases, however their molecular physio-pathology is not established yet.
Following the recent progress on this unique protein family and with new techniques becoming available, these are exciting times to study all aspects of TMEM16 physiology.
This Special Issue calls for original research, full reviews, and perspectives that address the current knowledge in the field of Ca2+-activated chloride channels and scramblases.Dr. Anna Boccaccio
Dr. Simone Pifferi
Manuscript Submission Information
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- Ion channels
- molecular mechanisms
- genetic disease
- Ca2+-activated chloride channels
- Phospholipid scramblase
- Ca2+-activated channels
- membrane asymmetry