Category: Neurological
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ADAM22: The Brain’s Gatekeeper
ADAM22 is a unique member of the ADAM family, primarily expressed in the brain. Unlike many of its relatives, ADAM22 is a non-catalytic metalloprotease-like protein, meaning it lacks proteolytic activity4. Picture ADAM22 as the bouncer at an exclusive neural nightclub. It’s involved in regulating cell adhesion and spreading, and it even plays a role in
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DMT1 aka DCT1 and NRAMP2
Natural resistance-associated macrophage protein 2 (NRAMP 2), also known as divalent metal transporter 1 (DMT1) and divalent cation transporter 1 (DCT1), is a protein that in humans is encoded by the SLC11A2 (solute carrier family 11, member 2) gene. DMT1 represents a large family of orthologous metal ion transporter proteins that are highly conserved from bacteria to humans. As its name suggests, DMT1 binds a variety of divalent metals
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Patent for protecting and treating organophosphate-induced neuronal injury with tobacco-derived cembranoids and analogues
Ford, Byron, Ferchmin Peter, Eterovic, Vesna, Methods and compositions for protecting and treating neuroinjury (Patent), United States Grant US-8530525-B2 Assignee: Central University of the Caribbean, Morehouse School of Medicine, Status: Active, Expires 2031-05-19, Document history 2013-09-10 Publication date, 2010-07-01 Filing date, 2009-07-14 Priority date. Funded by National Institute of Neurological Disorders and Stroke, National Institute on Minority Health and
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CBP has intrinsic acetyltransferase functions
Cyclic adenosine monophosphate Response Element Binding protein Binding Protein (CREB-binding protein), also known as CREBBP or CBP or KAT3A, is a coactivator encoded by the CREBBP gene in humans, located on chromosome 16p13.3. CBP has intrinsic acetyltransferase functions; it is able to add acetyl groups to both transcription factors as well as histone lysines, the latter of which has been shown to alter chromatin structure making genes more accessible for transcription. This relatively
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In mouse models of Alzheimer’s Disease, it has been shown that there is a decrease in neuronal histone acetylation, a critical function of CBP
Alzheimer’s Disease (AD) is a progressive neurodegenerative disease whose pathology is diagnosed based on the presence of neuritic amyloid beta (AÎČ) plaques and neurofibrillary tau (Ï) tangles. Because the exact causes of the disease are not clearly understood, there are a number of different mechanisms by which CBP (CREB-binding protein) is hypothesized to play a role
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Diminished CBP activity and decreased neuronal histone acetylation is associated with Huntington’s Disease
Huntington’s Disease (HD) is a fatal, progressing neurodegenerative disorder that is the result of a genetic mutation in the Huntingtin gene causing synthesis of a mutated huntingtin (Htt) protein. Symptoms most frequently associated with this disease are movement disorders, including impaired motor function, behavioral modification and cognitive impairment that ultimately results in dementia. It has been observed in animal
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Decreased concentrations of CBP and lower amounts of H3 and H4 acetylation associated with fetal alcohol spectrum disorders
Fetal alcohol spectrum disorders (FASD) is a classification of diseases that all result from alcohol exposure during pregnancy. Symptoms of these disorders include poor cerebellar-dependent learning, motor coordination and impaired balance. In rats with FASD, it was shown that they had decreased concentrations of CBP and lower amounts of H3 and H4 acetylation.
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