VEČEŘA, Josef, Eva BÁRTOVÁ, Jana KREJČÍ, Soňa LEGARTOVÁ, Denisa KOMŮRKOVÁ, Jana RUDÁ, Tibor ŠTARK, Eva DRAŽANOVÁ, Tomáš KAŠPÁREK, Alexandra ŠULCOVÁ, Frank J. DEKKER, Wiktor SZYMANSKI, Christian SEISER, Georg WEITZER, Raphael MECHOULAM, Vincenzo MICALE a Stanislav KOZUBEK. HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals. Journal of cellular physiology. United States: Wiley-Liss, 2018, roč. 233, č. 1, s. 530-548. ISSN 0021-9541. Dostupné z: https://dx.doi.org/10.1002/jcp.25914. |
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@article{1393528, author = {Večeřa, Josef and Bártová, Eva and Krejčí, Jana and Legartová, Soňa and Komůrková, Denisa and Rudá, Jana and Štark, Tibor and Dražanová, Eva and Kašpárek, Tomáš and Šulcová, Alexandra and Dekker, Frank J. and Szymanski, Wiktor and Seiser, Christian and Weitzer, Georg and Mechoulam, Raphael and Micale, Vincenzo and Kozubek, Stanislav}, article_location = {United States}, article_number = {1}, doi = {http://dx.doi.org/10.1002/jcp.25914}, keywords = {acetylome; H3K9 acetylation; HDACs; mouse neurogenesis; schizophrenia}, language = {eng}, issn = {0021-9541}, journal = {Journal of cellular physiology}, title = {HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals}, url = {http://dx.doi.org/10.1002/jcp.25914}, volume = {233}, year = {2018} }
TY - JOUR ID - 1393528 AU - Večeřa, Josef - Bártová, Eva - Krejčí, Jana - Legartová, Soňa - Komůrková, Denisa - Rudá, Jana - Štark, Tibor - Dražanová, Eva - Kašpárek, Tomáš - Šulcová, Alexandra - Dekker, Frank J. - Szymanski, Wiktor - Seiser, Christian - Weitzer, Georg - Mechoulam, Raphael - Micale, Vincenzo - Kozubek, Stanislav PY - 2018 TI - HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals JF - Journal of cellular physiology VL - 233 IS - 1 SP - 530-548 EP - 530-548 PB - Wiley-Liss SN - 00219541 KW - acetylome KW - H3K9 acetylation KW - HDACs KW - mouse neurogenesis KW - schizophrenia UR - http://dx.doi.org/10.1002/jcp.25914 N2 - Although histone acetylation is one of the most widely studied epigenetic modifications, there is still a lack of information regarding how the acetylome is regulated during brain development and pathophysiological processes. We demonstrate that the embryonic brain (E15) is characterized by an increase in H3K9 acetylation as well as decreases in the levels of HDAC1 and HDAC3. Moreover, experimental induction of H3K9 hyperacetylation led to the overexpression of NCAM in the embryonic cortex and depletion of Sox2 in the subventricular ependyma, which mimicked the differentiation processes. Inducing differentiation in HDAC1-deficient mouse ESCs resulted in early H3K9 deacetylation, Sox2 downregulation, and enhanced astrogliogenesis, whereas neuro-differentiation was almost suppressed. Neuro-differentiation of (wt) ESCs was characterized by H3K9 hyperacetylation that was associated with HDAC1 and HDAC3 depletion. Conversely, the hippocampi of schizophrenia-like animals showed H3K9 deacetylation that was regulated by an increase in both HDAC1 and HDAC3. The hippocampi of schizophrenia-like brains that were treated with the cannabinoid receptor-1 inverse antagonist AM251 expressed H3K9ac at the level observed in normal brains. Together, the results indicate that co-regulation of H3K9ac by HDAC1 and HDAC3 is important to both embryonic brain development and neuro-differentiation as well as the pathophysiology of a schizophrenia-like phenotype. ER -
VEČEŘA, Josef, Eva BÁRTOVÁ, Jana KREJČÍ, Soňa LEGARTOVÁ, Denisa KOMŮRKOVÁ, Jana RUDÁ, Tibor ŠTARK, Eva DRAŽANOVÁ, Tomáš KAŠPÁREK, Alexandra ŠULCOVÁ, Frank J. DEKKER, Wiktor SZYMANSKI, Christian SEISER, Georg WEITZER, Raphael MECHOULAM, Vincenzo MICALE a Stanislav KOZUBEK. HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals. \textit{Journal of cellular physiology}. United States: Wiley-Liss, 2018, roč.~233, č.~1, s.~530-548. ISSN~0021-9541. Dostupné z: https://dx.doi.org/10.1002/jcp.25914.
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