|Positive WB detected in||HeLa cells, Raji cells|
|Positive IP detected in||Raji cells|
|Positive IF detected in||HeLa cells|
|Western Blot (WB)||WB : 1:500-1:2000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:500-1:1000 for WB|
|Immunofluorescence (IF)||IF : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
17548-1-AP targets HDAC8 in WB, IP, IHC, IF,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||HDAC8 fusion protein Ag11696|
|Full Name||histone deacetylase 8|
|Calculated molecular weight||377 aa, 42 kDa|
|Observed molecular weight||49 kDa|
|GenBank accession number||BC050433|
|Gene ID (NCBI)||55869|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Histone deacetylases (HDAC) are a class of enzymes that remove the acetyl groups from the lysine residues leading to the formation of a condensed and transcriptionally silenced chromatin. At least 4 classes of HDAC were identified. As a class I HDAC, HDAC 8 was primarily found in the nucleus. It catalyzes the deacetylation of lysine residues in the histone N-terminal tails and represses transcription in large multiprotein complexes with transcriptional co-repressors. This antibody is a rabbit polyclonal antibody raised against full length HDAC8 of human origin.
Stabilized peptide HDAC inhibitors derived from HDAC1 substrate H3K56 for the treatment of cancer stem-like cells in vivo.
HDAC3 and HDAC8 are required for cilia assembly and elongation.
Chem Res Toxicol
Curcumin Derivative Epigenetically Reactivates Nrf2 Antioxidative Stress Signaling in Mouse Prostate Cancer TRAMP C1 Cells.
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Epigenetics reactivation of Nrf2 in Prostate TRAMP C1 Cells by curcumin analog FN1.
Downregulation of histone deacetylase 1 by microRNA-520h contributes to the chemotherapeutic effect of doxorubicin.
The triterpenoid corosolic acid blocks transformation and epigenetically reactivates Nrf2 in TRAMP-C1 prostate cells.