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Brm-HDAC3-Erm repressor complex suppresses dedifferentiation of intermediate neural progenitors back into type II neuroblasts.
Hdac3 served as an important regulator of the PI3K pathway and revealed a novel link between histone acetylation and growth control.
Overexpressing any of HDAC 3, 6, or 11 suppresses CGG repeat-induced neurodegeneration in a Drosophila model of fragile X (show FMR1 ELISA Kits) tremor ataxia (show USP14 ELISA Kits) syndrome.
) DHDAC1 (show HDAC1 ELISA Kits) and -3 have distinct functions in the control of gene expression
Mutant larvae display small imaginal discs, which result from abnormally elevated levels of apoptosis. This cell death occurs as a cell-autonomous response to HDAC3 loss and is accompanied by increased expression of the pro-apoptotic gene, hid.
Data suggest that complexes of HDAC3-H1.3 with NCOR1 and NCOR2/SMRT accumulate on chromatin in synchronized HeLa cells in late G2 phase and mitosis; deacetylation activity of HDAC3 is activated via phosphorylation of Ser-424 by CK2 only in mitosis.
this is the first report on the regulation mechanism of SIRT7 (show SIRT7 ELISA Kits) gene, in which, HDAC3 collaborated with C/EBPalpha (show CEBPA ELISA Kits) to occupy its responding element in the upstream region of SIRT7 (show SIRT7 ELISA Kits) gene and repressed its expression in human cells.
Among the class II HDACs, HDAC4 (show HDAC4 ELISA Kits) interacted with both MR and HDAC3 after aldosterone stimulation. The nuclear translocation of HDAC4 (show HDAC4 ELISA Kits) was mediated by protein kinase A (PKA) and protein phosphatases (PP)
miR (show MLXIP ELISA Kits)-335 exerted apoptotic effects and inhibited ubiquitination of HDAC3 in anti-cancer drug-resistant cancer cell lines. miR (show MLXIP ELISA Kits)-335 negatively regulated the invasion, migration, and growth rate of cancer cells.
ZBP-89 (show ZNF148 ELISA Kits) attenuates HDAC3 by increasing IkappaB degradation, dependent on Pin1 (show PIN1 ELISA Kits) but independent of NF-Kappab (show NFKB1 ELISA Kits)
Data suggest, in chronic hepatitis C virus infection, HDAC9 (histone deacetylase 9 (show HDAC9 ELISA Kits)) induction in liver regulates hepatic gluconeogenesis and systemic insulin (show INS ELISA Kits) resistance via deacetylation of FoxO1 (show FOXO1 ELISA Kits) (Forkhead box O 1) and HDAC3 (histone deacetylase 3).
These data suggest that HDAC3 indirectly modulates tubulin (show TUBB ELISA Kits) acetylation
The inhibition of the transcriptional activity of BCL9-2 (show BCL9L ELISA Kits) by WWOX (show WWOX ELISA Kits) and HDAC3 constitutes a new molecular mechanism and provides new insight for a broad range of cancers.
These observations suggested that HDAC3 plays an important role in the pathological courses of spinal cord injury by regulating miR (show MLXIP ELISA Kits)-130a expression
Time-course analysis revealed that HDAC6 (show HDAC6 ELISA Kits), HDAC3, and acetylated histone H3 (show HIST3H3 ELISA Kits) protein levels are significantly inhibited.
GC-induced direct repression, but not bindings of GR and of corepressors NCoR1 (show NCOR1 ELISA Kits)/SMRT, was abolished, indicating that HDAC3 is instrumental in IR nGRE-mediated repression
GR SUMOylation site is mandatory for the formation of a GR-small ubiquitin-related modifiers (SUMOs)-SMRT/NCoR1 (show NCOR1 ELISA Kits)-HDAC3 repressing complex, which is indispensable for NF-kappaB (show NFKB1 ELISA Kits)/AP1 (show JUN ELISA Kits)-mediated GC-induced tethered indirect transrepression in vitro
studies reveal an intricate epigenetic pathway where Hdac3 is required to repress miR-17-92 expression to allow for proper TGF-beta (show TGFB1 ELISA Kits) signaling during lung sacculation
Bach2 is suggested to cooperate with HDAC3-containing co-repressor complexes in B cells to regulate the stage-specific expression of Prdm1 (show PRDM1 ELISA Kits) by writing epigenetic modifications at the Prdm1 (show PRDM1 ELISA Kits) locus.
Hdac3 cooperates with p300 (show NOTCH1 ELISA Kits) to prime and maintain oligodendrocyte identity
Wild-type HDAC3 or catalytically inactive HDAC3 expression rescues aberrant endothelial-to-mesenchymal transition and epigenetic silencing of Tgf-beta1 (show TGFB1 ELISA Kits) in HDAC3-null outflow tracts and semilunar valves.
Study shows that conditional deletion of an epigenetic regulator, Hdac3, in osteoblast progenitor cells abrogates high fat diet-induced insulin (show INS ELISA Kits) resistance and hepatic steatosis. These Hdac3-deficient mice have reduced bone formation and lower circulating levels of total and undercarboxylated osteocalcin (show BGLAP ELISA Kits), coupled with decreased bone resorption activity.
These studies provide the first evidence for localization of HDAC3 at myofilaments and uncover a novel mechanism modulating the motor activity of cardiac MHC isoforms.
The study examined the physiological roles of Hdac3 by deletion of this gene during early thymocyte development using Lck (show LCK ELISA Kits)-Cre.
Results showed that the expression levels of HDAC1 (show HDAC1 ELISA Kits) and 3 are decreased gradually during embryonic stem cells (ESCs (show NR2E3 ELISA Kits)) mesodermal differentiation and interact physically with Bry protein, which is critical for mesodermal lineage commitment.
These results revealed a novel and specific role of hdac3 in liver development and the distinct functions between hdac1 (show HDAC1 ELISA Kits) and hdac3 in zebrafish embryonic development.
Histones play a critical role in transcriptional regulation, cell cycle progression, and developmental events. Histone acetylation/deacetylation alters chromosome structure and affects transcription factor access to DNA. The protein encoded by this gene belongs to the histone deacetylase/acuc/apha family. It has histone deacetylase activity and represses transcription when tethered to a promoter. It may participate in the regulation of transcription through its binding with the zinc-finger transcription factor YY1. This protein can also down-regulate p53 function and thus modulate cell growth and apoptosis. This gene is regarded as a potential tumor suppressor gene.
, histone Deacetylase-3
, histone deacetylase 3
, HDAC3 splicing HDAC3alpha
, HDAC3 splicing HDAC3beta
, HDAC3 splicing HDAC3delta
, HDAC3 splicing HDAC3gamma
, histone deacetylase-3