Articles tagged with Connexins
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Researchers found that a protein involved in ATP release, connexin 43, plays a key role in depressive- and anxiety-like behaviors. Restoring connexin 43 in the hippocampus improved behavioral outcomes and boosted ATP levels in stressed mice.
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.
Researchers found that deaf mice have nearly normal neural activity in the auditory system for two weeks after birth, suggesting a molecular mechanism for improved outcomes with early cochlear implants. This spontaneous activity helps train the brain to process sound before the ear canal opens.
Researchers have discovered a new strategy for treating arrhythmogenic cardiomyopathy by restoring the trafficking protein GJA1-20k, which enables healthy connections between heart cells. This finding may also be applicable to treating dangerous arrhythmias associated with other conditions.
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.
Researchers at VTC have developed a promising three-pronged approach to treating glioblastoma, a lethal brain cancer. By inhibiting two specific proteins with temozolomide, they created an effective 'triple combinational therapy' that overcame chemoresistance.
A team of Virginia Tech scientists has identified a new link between seizures and connexin 36 deficiency in zebrafish models. The study found that connexin 36 deficiency altered the susceptibility to neuronal hyperactivity, which may contribute to the onset of subsequent seizures.
Parkinson's disease can spread throughout the brain via tiny channels, where harmful protein aggregates bind and 'hitch a lift' with channel-forming proteins. This process involves specific proteins called connexins, which create small channels between cells.
A graduate student at Virginia Tech Carilion Research Institute is investigating how adenovirus affects gap junctions in the heart, which can lead to arrhythmia. The research aims to understand the pathways used by the virus in sudden cardiac death and potentially develop therapies for other forms of cardiac disease.
Scientists at Virginia Tech Carilion Research Institute have identified a novel cellular mechanism that can lead to cancer metastasis. The researchers found that the formation of gap junction structures allowing cells to communicate was disrupted during epithelial mesenchymal transition (EMT), despite an abundance of connexin 43 proteins.
Researchers developed a method to improve electrical transmission in the heart by introducing the Connexin 43 gene into cells forming the infarct scar. Mice with overexpressed Cx43 showed reduced cardiac arrhythmias compared to control animals.
Researchers at Kumamoto University successfully grafted human iPS cell-derived inner ear cells into embryonic mice, expressing key proteins essential for hearing development. The study's findings suggest that these cells may compensate for missing proteins and improve hearing loss in hereditary cases.
Researchers have identified a critical four-day period in fetal heart development that may help diagnose miscarriages. The study uses advanced imaging techniques to reveal the rapid organization of muscle tissue and cardiac fibres, shedding light on possible mechanisms behind failed heart formation.
Progeria, a rare genetic disease, is characterized by an elevated risk of arrhythmias and premature death due to anomalies in the transmission of electrical signals in the heart. The study reveals that mislocalization of connexin 43 reduces connectivity between cardiomyocytes, increasing the risk of arrhythmias.
Researchers from Virginia Tech Carilion Research Institute and clinicians have discovered a way to sensitize human glioblastoma cells to chemotherapy, offering new hope for patients with aggressive brain cancer. The breakthrough involves inhibiting connexin 43, a protein that facilitates cell signaling in damaged cells.
Researchers discovered connexin protein's ability to suppress cancer growth by tethering itself to cell-proliferating molecules. This finding could lead to new cancer therapies based on connexin molecules.
Researchers found that changes in occludin and connexin 43 expression are consistent with the development of brain edema, reflecting its pathogenesis. The study's findings may lead to better treatments for intracranial diseases.
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.
Brown University scientists discover a malaria drug that precisely blocks specific connexins in the brain and eye, which may help shed light on the cause of epilepsy and seizures. The breakthrough could also lead to new treatments for other neurological conditions.
Hopkins researchers identify connexin 43 gene as the cause of oculodentodigital dysplasia, a disorder affecting multiple body systems. The study reveals changes in the gene's sequence are responsible for the condition.