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Validated All-in-One™ qPCR Primer for HDAC3(NM_003883.3) Search again
Product ID:
HQP021612
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HD3, KDAC3, RPD3, RPD3-2
Gene Description:
histone deacetylase 3
Target Gene Accession:
NM_003883.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Histones play a critical role in transcriptional regulation, cell cycle progression, and developmental events.
Gene References into function
- Non-permissive cells contain the class I HDAC, HDAC3; super-expression of HDAC3 in normally permissive cells reduces infection and MIEP activity.
- Results show that the N-CoR-HDAC3 complex inhibits JNK activation through the associated GPS2 subunit and thus could potentially provide an alternative mechanism for hormone-mediated antagonism of AP-1 function.
- c-Jun phosporylation mediates dissociation of an inhibitory complex associated with HDAC3.
- N-CoR/histone deacetylase 3 complex is required for repression by thyroid hormone receptor
- the zinc fingers of nuclear receptors provide a general interaction interface for HDACs 3 and 4, recruiting HDACs 3 and 4 to the target DNA causing demonstrable histone deacetylation
- HDAC3 regulates osteoblast differentiation and bone formation; data show that HDAC3 actively regulates the transcriptional activity of the osteoblast master protein, Runx2.
- HDAC3 interacts directly and selectively with MAPK11/p38 beta isoform, represses ATF-2 transcriptional activity, and acts as a regulator of tumor necrosis factor gene expression in lipopolysaccharide-stimulated cells, especially in mononuclear phagocytes
- THAP7 coimmunoprecipitates with histone deacetylase 3 and the nuclear hormone receptor corepressor and represses transcription
- CMV IE1 interacts specifically with HDAC3 within infected cells, fundamental to transcriptional activation by IE1
- the N-CoR/HDAC3 complex has a role in regulating the expression of genes involved in circadian rhythm by functioning as corepressor for Rev-erbalpha
- Repression of Dlk1 requires HDAC3 deacetylase activity, which is recruited to the endogenous Dlk1 promoter where it interacts with KLF6. The interaction between HDAC3 and KLF6 is identified as a potential mechanism underlying adipogenesis.
- Elevated HDAC3 expression is associated with squamous cell lung carcinomas
- Data show that LAP2beta interacts at the nuclear envelope with HDAC3, a class-I histone deacetylase, and that TSA (an HDAC inhibitor) abrogates LAP2beta's transcriptional repressive activity.
- when complexed with Smad6, silences transcriptional activity of glucocorticoid receptor
- the inhibition of p15(INK4b) and p21(WAF1/cip1) may be one of the mechanisms by which HDAC3 participates in cell cycle regulation and oncogenesis
- PML-RARalpha functions by recruiting an HDAC3-MBD1 complex that contributes to the establishment and maintenance of the silenced chromatin state
- This study shows that SMRT/NCoR-HDAC3 complex is a cofactor of CNOT2-mediated repression and suggest that transcriptional regulation by the Ccr4-Not complex involves regulation of chromatin modification.
- Results provide evidence to show that the HDAC3/N-CoR co-repressor complex is involved in the aberrant transcription regulation in PML-RARalpha-expressing cells.
- beta-globin gene promoters in GM979 cells and in erythroid progenitors demonstrate that RB7 and butyrate induce dissociation of HDAC3.
- HDAC3 is a critical, transcription-independent regulator of mitosis.
- HDAC3 expression is elevated in human astrocytic tumours and its expression pattern is deregulated at the cellular level in high-grade gliomas.
- HDAC3 plays a significant role in the regulation of TNF-alpha-mediated VCAM-1 expression
- HDAC-3 cleavage is crucial for efficient apoptosis induction because it allows the activation of some proapoptotic genes during apoptosis progression.
- These results reveal an unexpected role for HDAC3 and suggest a novel pathway through which MEF2 activity is controlled in vivo.
- Histone deacetylase inhibitors transcriptionally inhibit agonist-induced tissue factor expression in endothelial cells and monocytes by a TF-kappaB- and HDAC3-dependent mechanism.
- High expression of HDAC3 is associated with cancer tissues
- data support a central role for HDAC3 in regulating the cell proliferation and differentiation of colon cancer cells and suggest a potential mechanism by which colon cancers may become resistant to luminal butyrate
- KLF4 might function as an activator or repressor of transcription depending on whether it interacts with co-activators such as p300 and CREB-binding protein or co-repressors such as HDAC3.
- the transcription factor YY1 binds to and recruits HDAC3 to the lanosterol synthase promoter.
- Runx2 and HDAC3 repress BSP gene expression and that this repression is suspended upon osteoblastic cell differentiation.
- pro-IL-16 forms a complex with GABPbeta1 and HDAC3 in suppressing the transcription of Skp2.
- we showed that the known effects of HDACs on differentiation and proliferation of cancer cells observed in vitro can also be confirmed in vivo.
- HDAC3 complex is involved in the formation of functional mitotic spindles and proper kinetochore-microtubule attachment
- Strong prognostic impact of HDAC isoforms in colorectal cancer.
- growth factors inhibit sumoylation of SREBPs through their phosphorylation, thus avoiding the recruitment of an HDAC3 corepressor complex and stimulating the lipid uptake and synthesis required for cell growth.
- Accessible chromatin-associated (histone 3 lysine 9) acetylation state serves as a cornerstone for differentially high expression of effector gene eomesodermin and its target genes perforin 1 and granzyme B in memory CD8 T cells.
- C-terminal region of p300 provides corepressor function and facilitates the recruitment of p300 and HDAC3 to the YY1-binding site and represses the c-Myc promoter.
- Studies show that cancer cells effectively maintain low levels of pyruvate to prevent inhibition of HDAC1/HDAC3 and thereby to evade cell death.
- role of histone deacetylase 3 (HDAC3) in sister chromatid cohesion and the deacetylation of histone H3 Lys 4 (H3K4) at the centromere
- P/CAF deacetylation by HDAC3 and in a minor degree by HDAC1, HDAC2, or HDAC4 leads to cytoplasmic accumulation of P/CAF.
- These results indicate that HDAC3 may act as a scaffold protein for PP2A to regulate the LIF/STAT3-mediated signaling pathway.