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Endothelial-Mesenchymal Transition is initiated by recruitment of aberrantly phosphorylated DNMT1 (show DNMT1 ELISA Kits) to the RASAL1 (show RASAL1 ELISA Kits) CpG island promoter by HDAC2, causing aberrant promoter methylation and transcriptional suppression.
Selective inhibition of HDAC2 in lung tumor cell causes survivin (show BIRC5 ELISA Kits) downregulation through activation of p53 (show TP53 ELISA Kits), which is mediated by downregulation of Mdm2 (show MDM2 ELISA Kits).
our study revealed that HDAC2 is overexpressed in colorectal cancer (CRC (show CALR ELISA Kits)) cells; its knockdown can increase the sensitivity of CRC (show CALR ELISA Kits) cells to doxorubicin via upregulation of ABCB1 (show ABCB1 ELISA Kits)
Pancreatic adenocarcinoma patients with enhanced HDAC-1 (show HDAC1 ELISA Kits) and -6 expression showed significantly longer survival times compared to those with low expression, while a borderline association concerning HDAC-2 expression was noted.
Lymphocyte senescence in COPD (show ARCN1 ELISA Kits) is associated with loss of HDAC2 in CD28nullCD8+ T and NKT (show SLC22A6 ELISA Kits)-like cells.
Results show that mRNA expression of histone deacetylases HDAC1 (show HDAC1 ELISA Kits) and HDAC2 were significantly increased in peripheral blood mononuclear cells of patients with with Graves' disease compared to controls.
HDAC2 may not confer susceptibility to Schizophrenia in Han Chinese.
In endothelial dysfunction, HDAC2 levels were reciprocally regulated by ectopic expression of NEDD8 (show NEDD8 ELISA Kits) and the de-NEDDylating enzyme SENP8 (show SENP8 ELISA Kits).
shRNA-mediated knockdown of HDAC1 (show HDAC1 ELISA Kits) or HDAC2 resulted in growth inhibition of B-cell acute lymphoblastic leukemia cells.
Aberrant overexpression of HDACs in basal cells of IPF lungs may contribute to the bronchiolisation process in this disease. Similarly, generation and apoptosis resistance of IPF fibroblasts are mediated by enhanced activity of HDAC (show HDAC3 ELISA Kits) enzymes.
Our data show that: i) HDAC2 levels and activity are increased in NPC (show NPC1 ELISA Kits) neuronal models and in Npc1 (show NPC1 ELISA Kits)(-/-) mice; ii) inhibition of c-Abl (show ABL1 ELISA Kits) or c-Abl (show ABL1 ELISA Kits) deficiency prevents the increase of HDAC2 protein levels and activity in NPC (show NPC1 ELISA Kits) neuronal models
This study reveals a dominant negative effect of catalytically inactive HDAC2 on specific corepressor complexes resulting in histone hyperacetylation, transcriptional derepression, and, ultimately, perinatal lethality.
This study demonstrated that hdac2 increase in skeletal muscle in muscle atrophy.
Intestinal epithelial cell (IEC) determination and intestinal homeostasis are highly dependent on Hdac1 (show HDAC1 ELISA Kits) and Hdac2 activity levels, and changes in the IEC acetylome may alter the mucosal environment.
results demonstrate that combined HDAC1 (show HDAC1 ELISA Kits) and HDAC2 ablation promotes survival of axotomized retinal ganglion cells; HDAC1 (show HDAC1 ELISA Kits)/2 ablation inhibited the apoptotic pathway by impairing acetylation status of p53 (show TP53 ELISA Kits) and reducing PUMA (show BBC3 ELISA Kits) expression, thereby contributing to the ensuing enhanced neuroprotection due to HDAC1 (show HDAC1 ELISA Kits)/2 depletion
Scopolamine induced memory impairment along with increased gene expression of HDAC2 in corpus striatum.
mechanistic evidence for the gene-specific transcription repression activity of Tet2 (show TET2 ELISA Kits) via histone deacetylation and for the prevention of constant transcription activation at the chromatin level for resolving inflammation
HDAC2 might be a downstream effector of Jak2 (show JAK2 ELISA Kits) to mediate cardiac hypertrophic response by pressure overload or Ang-II (show AGT ELISA Kits).
Hdac1 (show HDAC1 ELISA Kits) and Hdac2 are crucial for kidney development, regulating Wnt (show WNT2 ELISA Kits) and p53 (show TP53 ELISA Kits) pathways in the ureteric bud epithelium.
Report role of myocardial mSin3A/HDAC1 (show HDAC1 ELISA Kits)/2 complex in mediating the beneficial effects of exercise in diabetic cardiomyopathy.
This gene product belongs to the histone deacetylase family. Histone deacetylases act via the formation of large multiprotein complexes, and are responsible for the deacetylation of lysine residues at the N-terminal regions of core histones (H2A, H2B, H3 and H4). This protein forms transcriptional repressor complexes by associating with many different proteins, including YY1, a mammalian zinc-finger transcription factor. Thus, it plays an important role in transcriptional regulation, cell cycle progression and developmental events. Alternative splicing results in multiple transcript variants.
YY1-associated factor 1
, transcriptional regulator homolog RPD3
, YY1 transcription factor-binding protein
, histone deacetylase-2