Articles tagged with Hemichannels
Researchers from PSI and ETH Zurich studied connexin-36 gap junction channels and found that antimalarial drug mefloquine binds to the channels, potentially explaining its severe side effects. The study provides new insights into how drugs interact with connexins and may lead to the development of therapies for neurological diseases.
A research team led by City University of Hong Kong neuroscientist Dr. Geoffrey Lau Chun-yue identified a new drug candidate, D4, that selectively blocks connexin hemichannels to suppress neuroinflammation and curbs TLE seizures in a mouse model. The findings suggest a promising new treatment strategy for epilepsy.
Scientists have identified connexin (Cx) 43 hemichannels on the surface of bone cells as a potential new target for medications to treat osteoporosis and other conditions that cause bone loss. The study, published in eLife, reveals how these channels play a crucial role in responding to mechanical stress and building stronger bones.
Researchers developed a new approach to treat ischemic strokes by blocking hemichannels, reducing brain damage. The approach also showed potential for treating other neurodegenerative conditions.
A study published in The Journal of General Physiology found that two specific mutations in the Cx26 protein cause distinct symptoms in KID Syndrome patients. Hemichannels containing the N14Y mutation showed lower ion conductance, while those with the N14K mutation were more stable and allowed robust ion conductance.
A new study advances our understanding of connexin hemichannel closure by elucidating the loop gating mechanism. The research also sheds light on the conformational changes occurring within the loop gate, providing a clearer picture of how these channels are kept closed.
Researchers at University of British Columbia have identified hemichannels as a potential target for treating epileptic seizures caused by brain trauma or stroke. Blocking these channels may lead to the development of new therapies for epilepsy patients.
Researchers discover a poorly understood mechanism linking smoking to lung damage, where toxins in cigarette smoke open unpaired hemichannels that lead to rapid cell death. Drugs preventing hemichannel opening offer new ways to prevent cellular damage and potentially treat diseases tied to oxidative stress.