Special Issue "Gap Junction Channels and Hemichannels in Health and Disease"
Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 7021
Interests: Gap junctions; connexins; cell communication; calmodulin; calcium; channel gating
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Special Issue in International Journal of Molecular Sciences: Chemical Regulation of Gap Junction Channels and Hemichannels 2.0
Special Issue in International Journal of Molecular Sciences: Gap Junction Channels and Hemichannels in Health and Disease 2.0
2. Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy
Interests: biophysics; neuropathies; Charcot-Marie-Tooth; connexin 32; brain organoids; electrophysiology; live imaging; systems biology
Neighboring cells directly exchange small cytosolic molecules via cell–cell channels clustered at gap junctions. Gap junction-mediated cell communication is a very important mechanism that allows cells to coordinate numerous functions. Conversely, impaired cell–cell communication is known to cause many diseases.
Each gap junction channel is formed by the interaction of two hemichannels that create a hydrophilic pathway spanning the two plasma membranes and a narrow extracellular space (gap). In turn, each hemichannel is an oligomer of six proteins (connexins/innexins). Gap junction channels are regulated by a gating mechanism sensitive to changes in cytosolic calcium (Ca2+i) and pHi.
In the mid-1980s, the cloning of connexin/innexin cDNAs opened the way to the field of gap junction channelopathies. Thus far, at least thirty-five genetic diseases caused by mutations of eleven different connexins genes are known to cause numerous structural and functional defects in the central and peripheral nervous system as well as in the heart, skin, eyes, teeth, ears, bone, hair, nails, and lymphatic system.
While all of these diseases are due to connexin mutations, minimal attention has thus far been addressed to potential diseases caused by mutations of connexin-associated molecules. An important accessory of gap junctions is the protein calmodulin (CaM), which plays a role in channel gating and is relevant to gap junction formation as well. Recently, diseases caused by CaM mutations (calmodulinopathies) have been identified, but thus far, calmodulinopathy studies have not considered the potential effect of CaM mutations on gap junction function. Therefore, it is important to also raise awareness on the likely role of CaM mutations in defects of gap-junction-mediated cell communication.
Prof. Dr. Camillo Peracchia
Dr. Mario Bortolozzi
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- gap junction channel