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This new volume of Methods in Enzymology continues the legacy of this premier serial by containing quality chapters authored by leaders in the field. This volume covers G protein coupled receptors and includes chapters on such topics as post-translation modification of GPCR in relationship to biased agonism, structure-based virtual screening, and GPCR oligomerization in the brain. Continues the legacy of this premier serial with quality chapters authored by leaders in the fieldCovers G protein coupled receptorsContains chapters on such topics as p
Cochlear nucleus. --- Neural transmission -- Regulation. --- Receptors, Cell Surface --- Membrane Proteins --- Proteins --- Amino Acids, Peptides, and Proteins --- Chemicals and Drugs --- Receptors, G-Protein-Coupled --- Human Anatomy & Physiology --- Health & Biological Sciences --- Animal Biochemistry --- G proteins. --- Cell receptors. --- Cellular signal transduction. --- Cellular information transduction --- Information transduction, Cellular --- Signal transduction, Cellular --- Cell membrane receptors --- Cell surface receptors --- Receptors, Cell --- GTP-binding proteins --- GTP regulatory proteins --- Guanine nucleotide-binding proteins --- Guanine nucleotide regulatory proteins --- Bioenergetics --- Cellular control mechanisms --- Information theory in biology --- Binding sites (Biochemistry) --- Cell membranes --- Membrane proteins --- G proteins --- Enzymology. --- Receptors.
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The sense of hearing is vulnerable to environmental challenges, such as exposure to noise. More than 1.5 billion people experience some decline in hearing ability during their lifetime, of whom at least 430 million will be affected by disabling hearing loss. If not identified and addressed in a timely way, hearing loss can severely reduce the quality of life at various stages. Some causes of hearing loss can be prevented, for example from occupational or leisure noise. The World Health Organization estimates that more than 1 billion young people put themselves at risk of permanent hearing loss by listening to loud music over long periods of time. Mitigating such risks through public health action is essential to reduce the impact of hearing loss in the community. The etiology of sensorineural hearing loss is complex and multifactorial, arising from congenital and acquired causes. This book highlights the diverse range of approaches to sensorineural hearing loss, from designing new animal models of age-related hearing loss, to the use of microRNAs as biomarkers of cochlear injury and drug repurposing for the therapy of age-related and noise-induced hearing loss. Further investigation into the underlying molecular mechanisms of sensorineural hearing loss and the integration of the novel drug, cell, and gene therapy strategies into controlled clinical studies will permit significant advances in a field where there are currently many unmet needs.
Medicine --- brain-derived neurotrophic factor --- TrkB --- inner ear --- development --- zebrafish --- mitochondria dysfunction --- reactive oxygen species --- hypoxic --- d-galactose --- high-fat diet --- aging --- hearing loss --- astrocytes --- auditory brainstem --- lateral superior olive --- gap junctions --- voltage-activated calcium channel 1.3 --- otoferlin --- spontaneous activity --- deafness --- circadian dysregulation --- clock genes --- noise-induced hearing loss --- sensory hair cells --- synaptic ribbons --- sensorineural hearing loss --- hyperbaric oxygenation --- adjunctive therapy --- microRNAs --- cochlear nucleus --- inferior colliculus --- neuroplasticity --- noise-induced cochlear injury --- cochlear rescue --- otoprotection --- adenosine A1 receptor --- regulator of G protein signalling 4 --- CCG-4986 --- intratympanic drug delivery --- potassium voltage-gated channel subfamily q member 4 --- potassium --- nonsyndromic hearing loss --- KCNQ4 activator --- age-related hearing loss --- selegiline --- chronic oral treatment --- hearing protection --- mouse model --- brain-derived neurotrophic factor --- TrkB --- inner ear --- development --- zebrafish --- mitochondria dysfunction --- reactive oxygen species --- hypoxic --- d-galactose --- high-fat diet --- aging --- hearing loss --- astrocytes --- auditory brainstem --- lateral superior olive --- gap junctions --- voltage-activated calcium channel 1.3 --- otoferlin --- spontaneous activity --- deafness --- circadian dysregulation --- clock genes --- noise-induced hearing loss --- sensory hair cells --- synaptic ribbons --- sensorineural hearing loss --- hyperbaric oxygenation --- adjunctive therapy --- microRNAs --- cochlear nucleus --- inferior colliculus --- neuroplasticity --- noise-induced cochlear injury --- cochlear rescue --- otoprotection --- adenosine A1 receptor --- regulator of G protein signalling 4 --- CCG-4986 --- intratympanic drug delivery --- potassium voltage-gated channel subfamily q member 4 --- potassium --- nonsyndromic hearing loss --- KCNQ4 activator --- age-related hearing loss --- selegiline --- chronic oral treatment --- hearing protection --- mouse model
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The sense of hearing is vulnerable to environmental challenges, such as exposure to noise. More than 1.5 billion people experience some decline in hearing ability during their lifetime, of whom at least 430 million will be affected by disabling hearing loss. If not identified and addressed in a timely way, hearing loss can severely reduce the quality of life at various stages. Some causes of hearing loss can be prevented, for example from occupational or leisure noise. The World Health Organization estimates that more than 1 billion young people put themselves at risk of permanent hearing loss by listening to loud music over long periods of time. Mitigating such risks through public health action is essential to reduce the impact of hearing loss in the community. The etiology of sensorineural hearing loss is complex and multifactorial, arising from congenital and acquired causes. This book highlights the diverse range of approaches to sensorineural hearing loss, from designing new animal models of age-related hearing loss, to the use of microRNAs as biomarkers of cochlear injury and drug repurposing for the therapy of age-related and noise-induced hearing loss. Further investigation into the underlying molecular mechanisms of sensorineural hearing loss and the integration of the novel drug, cell, and gene therapy strategies into controlled clinical studies will permit significant advances in a field where there are currently many unmet needs.
Medicine --- brain-derived neurotrophic factor --- TrkB --- inner ear --- development --- zebrafish --- mitochondria dysfunction --- reactive oxygen species --- hypoxic --- d-galactose --- high-fat diet --- aging --- hearing loss --- astrocytes --- auditory brainstem --- lateral superior olive --- gap junctions --- voltage-activated calcium channel 1.3 --- otoferlin --- spontaneous activity --- deafness --- circadian dysregulation --- clock genes --- noise-induced hearing loss --- sensory hair cells --- synaptic ribbons --- sensorineural hearing loss --- hyperbaric oxygenation --- adjunctive therapy --- microRNAs --- cochlear nucleus --- inferior colliculus --- neuroplasticity --- noise-induced cochlear injury --- cochlear rescue --- otoprotection --- adenosine A1 receptor --- regulator of G protein signalling 4 --- CCG-4986 --- intratympanic drug delivery --- potassium voltage-gated channel subfamily q member 4 --- potassium --- nonsyndromic hearing loss --- KCNQ4 activator --- age-related hearing loss --- selegiline --- chronic oral treatment --- hearing protection --- mouse model --- n/a
Choose an application
The sense of hearing is vulnerable to environmental challenges, such as exposure to noise. More than 1.5 billion people experience some decline in hearing ability during their lifetime, of whom at least 430 million will be affected by disabling hearing loss. If not identified and addressed in a timely way, hearing loss can severely reduce the quality of life at various stages. Some causes of hearing loss can be prevented, for example from occupational or leisure noise. The World Health Organization estimates that more than 1 billion young people put themselves at risk of permanent hearing loss by listening to loud music over long periods of time. Mitigating such risks through public health action is essential to reduce the impact of hearing loss in the community. The etiology of sensorineural hearing loss is complex and multifactorial, arising from congenital and acquired causes. This book highlights the diverse range of approaches to sensorineural hearing loss, from designing new animal models of age-related hearing loss, to the use of microRNAs as biomarkers of cochlear injury and drug repurposing for the therapy of age-related and noise-induced hearing loss. Further investigation into the underlying molecular mechanisms of sensorineural hearing loss and the integration of the novel drug, cell, and gene therapy strategies into controlled clinical studies will permit significant advances in a field where there are currently many unmet needs.
brain-derived neurotrophic factor --- TrkB --- inner ear --- development --- zebrafish --- mitochondria dysfunction --- reactive oxygen species --- hypoxic --- d-galactose --- high-fat diet --- aging --- hearing loss --- astrocytes --- auditory brainstem --- lateral superior olive --- gap junctions --- voltage-activated calcium channel 1.3 --- otoferlin --- spontaneous activity --- deafness --- circadian dysregulation --- clock genes --- noise-induced hearing loss --- sensory hair cells --- synaptic ribbons --- sensorineural hearing loss --- hyperbaric oxygenation --- adjunctive therapy --- microRNAs --- cochlear nucleus --- inferior colliculus --- neuroplasticity --- noise-induced cochlear injury --- cochlear rescue --- otoprotection --- adenosine A1 receptor --- regulator of G protein signalling 4 --- CCG-4986 --- intratympanic drug delivery --- potassium voltage-gated channel subfamily q member 4 --- potassium --- nonsyndromic hearing loss --- KCNQ4 activator --- age-related hearing loss --- selegiline --- chronic oral treatment --- hearing protection --- mouse model --- n/a
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