Membrane Channels in Intercellular Communication
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".
Deadline for manuscript submissions: 31 August 2025 | Viewed by 76
Special Issue Editors
Interests: Gap junctions; connexins; cell communication; calmodulin; calcium; channel gating
Special Issues, Collections and Topics in MDPI journals
Interests: gap junctions and hemichannels; connexins; signaling transmission; breast cancer; osteosarcoma; metastasis
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Most vertebrate and invertebrate cells exchange ions and small cytosolic molecules directly via cell–cell channels that are clustered at gap junctions. Gap junction-mediated cell–cell communication is an important mechanism that allows cells to maintain homeostasis and coordinate numerous functions. Conversely, blocked cell–cell communication, known as cell–cell uncoupling, is known to cause many diseases. Each gap junction channel is formed by the interaction of two hemichannels, which create a hydrophilic pathway that spans both plasma membranes and the narrow extracellular space (gap). In turn, each hemichannel is an oligomer of six proteins, known as connexins in vertebrates and innexins in invertebrates. Gap junction channels are regulated by gating mechanisms that are sensitive to changes in cytosolic calcium (Ca2+i), pHi, and membrane potential and trans junctional voltage (Vj) gradients. In the mid-1980s, the cloning of connexin/innexin cDNAs paved the way for the study of gap junction channelopathies. To date, at least thirty-five genetic diseases caused by mutations of eleven different connexins genes have been identified; they are known to result in 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 these diseases are caused by connexin mutations, minimal attention has been given to potential diseases caused by mutations of connexin-associated molecules. An important accessory of gap junctions is the protein calmodulin (CaM), a highly sensitive modulator of Ca2+i known to play a key role in channel gating and gap junction formation. Other important accessory proteins are enzymes like kinases and phosphatases which, respectively, phosphorylate and dephosphorylate connexins, altering channel permeability and affecting connexin assembly into hemichannels.
This issue aims to publish review articles and/or original papers that highlight important findings on the functions of direct cell–cell communication and the pathological consequences of connexin mutations. It will also explore hypotheses, speculations, suggestions, and ideas that can be tested experimentally.
Prof. Dr. Camillo Peracchia
Prof. Dr. Jean Jiang
Guest Editors
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Keywords
- gap junctions
- connexins
- innexins
- channels
- hemichannels
- connexin mutations
- channel gating
- chemical gating
- voltage gating
- cell–cell coupling
- cell-cell uncoupling
- cell communication
- intercellular communication
- calcium
- pH
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