ArticleBiology2023
Deletion of the Neuronal Transcription Factor Satb1 Induced Disturbance of the Kinome and Mechanisms of Hypoxic Preconditioning.
Article in Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Hippocampal Gene Expression in Zebra Finches Reveals Sex- and Subregion-Specific Topographies.eNeuro · 2026Article
- Opposite Effects of Small and Large Diameter Selenium Nanoparticles on the Redox-Status and Survival of Cortical Cells in Toxic Models In Vitro.Biological trace element research · 2026Article
- Cluster Headache and Hypoxia: Breathing New Life into an Old Theory, with Novel Implications.Neurology international · 2024Review
- Generation and Characterization of Three Novel Mouse Mutant Strains Susceptible to Audiogenic Seizures.Cells · 2024Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Genetic disorders affecting the functioning of the brain lead not only to the development of numerous hereditary diseases but also to the development of neurodegenerative and cognitive disorders. The result of this may be the disability of part of the able-bodied population. Almost all pathological states of the brain are characterized by serious defects in the intracellular and intercellular signaling of neurons and glial cells. At the same time, the mechanisms of disruption of these signaling cascades are not well understood due to the large number of molecules, including transcription factors that, when mutated, cause brain malformations. The transcription factor Satb1 is one of the least studied factors in the cerebral cortex, and the effects of its deletion in the postnatal brain are practically not studied. Hyperexcitability of neurons is observed in many genetic diseases of the nervous system (Hirschsprung's disease, Martin-Bell syndrome, Huntington's disease, Alzheimer's, etc.), as well as in ischemic brain phenomena and convulsive and epileptic conditions of the brain. In turn, all these disorders of brain physiology are associated with defects in intracellular and intercellular signaling and are often the result of genetic disorders. Using Satb1 mutant mice and calcium neuroimaging, we show that Satb1 deletion in projection neurons of the neocortex causes downregulation of protein kinases PKC, CaMKII, and AKT/PKB, while a partial deletion does not cause a dramatic disruption of kinome and Ca
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