Results 61 to 70 of about 98,638 (334)

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

open access: yesMolecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto   +13 more
wiley   +1 more source

Microbiota derived short chain fatty acids promote histone crotonylation in the colon through histone deacetylases

open access: yesNature Communications, 2018
Histone post-translational modifications are known key regulators of gene expression. Here, the authors characterize histone crotonylation at histone H3 lysine 18 in intestinal epithelia and find that it is a highly dynamic cell cycle regulated mark ...
Rachel Fellows   +25 more
doaj   +1 more source

TdIF1 recognizes a specific DNA sequence through its Helix-Turn-Helix and AT-hook motifs to regulate gene transcription [PDF]

open access: yes, 2013
Peer reviewedPublisher ...
Hori, Katsutoshi   +4 more
core   +3 more sources

ATF4‐mediated stress response as a therapeutic vulnerability in chordoma

open access: yesMolecular Oncology, EarlyView.
We screened 5 chordoma cell lines against 100+ inhibitors of epigenetic and metabolic pathways and kinases and identified halofuginone, a tRNA synthetase inhibitor. Mechanistically halofuginone induces an integrated stress response, with eIF2alpha phosphorylation, activation of ATF4 and its target genes CHOP, ASNS, INHBE leading to cell death ...
Lucia Cottone   +11 more
wiley   +1 more source

HDAC inhibition is associated to valproic acid induction of early megakaryocytic markers [PDF]

open access: yes, 2006
Valproic acid (VPA), a histone deacetylase inhibitor, causes differentiation in different cell lines and in a cell-specific manner; yet, its effect on megakaryocytic (MK) differentiation has not been studied.
Ciccarelli, Carmela   +9 more
core  

Chromatin status and transcription factor binding to gonadotropin promoters in gonadotrope cell lines. [PDF]

open access: yes, 2017
BackgroundProper expression of key reproductive hormones from gonadotrope cells of the pituitary is required for pubertal onset and reproduction. To further our understanding of the molecular events taking place during embryonic development, leading to ...
Brayman, Melissa J   +6 more
core   +3 more sources

SIRT4 positively regulates autophagy via ULK1, but independently of HDAC6 and OPA1

open access: yesFEBS Open Bio, EarlyView.
Cells expressing SIRT4 (H161Y), a catalytically inactive mutant of the sirtuin SIRT4, fail to upregulate LC3B‐II and exhibit a reduced autophagic flux under stress conditions. Interestingly, SIRT4(H161Y) promotes phosphorylation of ULK1 at S638 and S758 that are associated with inhibition of autophagy initiation.
Isabell Lehmkuhl   +13 more
wiley   +1 more source

Unmasking the biological function and regulatory mechanism of NOC2L: a novel inhibitor of histone acetyltransferase

open access: yesJournal of Translational Medicine, 2023
NOC2 like nucleolar associated transcriptional repressor (NOC2L) was recently identified as a novel inhibitor of histone acetyltransferase (INHAT).
Siyi Lu   +3 more
doaj   +1 more source

Histone deacetylase adaptation in single ventricle heart disease and a young animal model of right ventricular hypertrophy. [PDF]

open access: yes, 2017
BackgroundHistone deacetylase (HDAC) inhibitors are promising therapeutics for various forms of cardiac diseases. The purpose of this study was to assess cardiac HDAC catalytic activity and expression in children with single ventricle (SV) heart disease ...
A Cevik   +49 more
core   +1 more source

Histone deacetylases and cancer [PDF]

open access: yesOncogene, 2007
Histone deacetylases (HDACs) regulate the expression and activity of numerous proteins involved in both cancer initiation and cancer progression. By removal of acetyl groups from histones, HDACs create a non-permissive chromatin conformation that prevents the transcription of genes that encode proteins involved in tumorigenesis. In addition to histones,
M A, Glozak, E, Seto
openaire   +2 more sources

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