https://transhumanist.ru/index.php?action=history&feed=atom&title=AKAP12 2026-06-17T12:32:26Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=AKAP12&diff=5847&oldid=prev 2021-05-12T14:56:09Z

<p>Новая страница: «A-kinase anchor protein 12 (AKAP-12) (A-kinase anchor protein 250 kDa) (AKAP 250) (Gravin) (Myasthenia gravis autoantigen) [AKAP250] ==Publications== {{medline-...»</p> <p><b>Новая страница</b></p><div>A-kinase anchor protein 12 (AKAP-12) (A-kinase anchor protein 250 kDa) (AKAP 250) (Gravin) (Myasthenia gravis autoantigen) [AKAP250]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=A-Kinase Anchor Protein 12 Is Required for Oligodendrocyte Differentiation in Adult White Matter.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29314444<br /> |abstract=Oligodendrocyte precursor cells (OPCs) give rise to oligodendrocytes in cerebral white matter. However, the underlying mechanisms that regulate this process remain to be fully defined, especially in adult brains. Recently, it has been suggested that signaling via A-kinase anchor protein 12 ([[AKAP12]]), a scaffolding protein that associates with intracellular molecules such as protein kinase A, may be involved in Schwann cell homeostasis and peripheral myelination. Here, we asked whether [[AKAP12]] also regulates the mechanisms of myelination in the CNS. [[AKAP12]] knockout mice were compared against wild-type (WT) mice in a series of neurochemical and behavioral assays. Compared with WTs, 2-months old [[AKAP12]] knockout mice exhibited loss of myelin in white matter of the corpus callosum, along with perturbations in working memory as measured by a standard Y-maze test. Unexpectedly, very few OPCs expressed [[AKAP12]] in the corpus callosum region. Instead, pericytes appeared to be one of the major [[AKAP12]]-expressing cells. In a cell culture model system, conditioned culture media from normal pericytes promoted in-vitro OPC maturation. However, conditioned media from [[AKAP12]]-deficient pericytes did not support the OPC function. These findings suggest that [[AKAP12]] signaling in pericytes may be required for OPC-to-oligodendrocyte renewal to maintain the white matter homeostasis in adult brain. Stem Cells 2018;36:751-760.<br /> |mesh-terms=* A Kinase Anchor Proteins<br /> * Aging<br /> * Animals<br /> * Cell Cycle Proteins<br /> * Cell Differentiation<br /> * Cell Proliferation<br /> * Cells, Cultured<br /> * Culture Media, Conditioned<br /> * Mice, Knockout<br /> * Myelin Sheath<br /> * Neural Stem Cells<br /> * Neurogenesis<br /> * Oligodendroglia<br /> * White Matter<br /> |keywords=* A-kinase anchor protein 12<br /> * Oligodendrocyte<br /> * Oligodendrocyte precursor cell<br /> * Pericytes<br /> * White matter<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5918158<br /> }}</div>

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