|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, 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.
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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.