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Validated All-in-One™ qPCR Primer for HDAC4(NM_006037.3) Search again
Product ID:
HQP023167
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AHO3, BDMR, HA6116, HD4, HDAC-4, HDAC-A, HDACA, NEDCHF, NEDCHID
Gene Description:
histone deacetylase 4
Target Gene Accession:
NM_006037.3(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
- HDAC4 is primarily a cytoplasmic resident protein, requiring a trans-acting nuclear localization signal for nuclear localization.
- The SUMO E3 ligase RanBP2 promotes modification of the HDAC4 deacetylase
- MITR, HDAC4, and HDAC5 associate with heterochromatin protein 1 (HP1), an adaptor protein that recognizes methylated lysines within histone tails and mediates transcriptional repression by recruiting histone methyltransferase
- This protein interacts with 53BP1 to mediate DNA damage response.
- full-length HDAC4 can repress MEF2 through multiple independent repressive domains
- 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
- caspases could specifically modulate gene repression and apoptosis through the proteolyic processing of HDAC4
- ICP0 of herpes simplex virus type 1 interacts with and controls the repressor activity of class II HDAC4
- HDAC4 has a role in cell death and differentiation
- data indicate that recruitment of HDAC4 is necessary for PLZF-mediated repression in both normal and leukaemic cells
- HDAC4 regulates ERalpha activity as a N-terminal coregulator.
- histone deacetylase 4- and SIRT1 deacetylase-mediated lysine modifications regulate MEF2
- Results show that calcium/calmodulin-dependent kinase II (CaMKII) signals specifically to histone deacetylase (HDAC)4 by binding to a unique docking site that is absent in other class IIa HDACs.
- HDAC4 (histone deacetylase 4) and p300, a known HAT (histone acetyltransferase), reversibly controlled the activity of the IL-5 promoter in vivo and in vitro, with a concurrent alteration of histone H3 acetylation status at the promoter regions.
- HDAC4 as a specific downstream substrate of CaMKIIdeltaB in cardiac cells and have broad applications for the signaling pathways leading to cardiac hypertrophy and heart failure.
- crystallographic analysis of the N-terminal domain of histone deacetylase 4
- Results show that both JARID1B and HDAC4 expressed in breast cancers.
- expression of the silencing mediator of retinoid and thyroid receptor (SMRT) & histone deacetylase4 (HDAC4) enhances formation of Bach2 foci in nuclear matrix. SMRT mediates HDAC4 binding to Bach2, & HDAC4 facilitates retention of Bach2 in the foci.
- HDAC4 is an essential epigenetic regulator of MF differentiation and HDAC4 is a potential target for treating MF-related disorders.
- Data suggest that, through specific posttranslation modifications, extracellular signals control two distinct nuclear pools of HDAC4 to differentially dictate cell death and differentiation.
- Results show that recruitment of histone deacetylase 4 is involves the CRIF1-mediated inhibition of AR transactivation.
- NO-dependent PP2A activation plays a key role in nuclear translocation of class II HDACs HDAC4 and HDAC5
- These observations suggest that PP2A, via the dephosphorylation of multiple serines including the 14-3-3 binding sites and serine 298, controls HDAC4 nuclear import.
- These findings revealed that TNF-alpha induced VCAM-1 expression via multiple signaling pathways.
- Structural and functional analysis of the human HDAC4 catalytic domain reveals a regulatory structural zinc-binding domain
- HDAC4 is a novel regulator of colon cell proliferation through repression of p21
- This study showed that in skeletal muscle, HDAC4 is a critical modulator of MEF2-dependent structural and contractile gene expression in response to neural activity.
- Analysis of a series of HDAC4 mutants by nuclear import assay suggested that phosphorylation and subsequent 14-3-3 binding reduce nuclear import rather than enhancing nuclear export.
- 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 HDAC4 and HDAC5 increase the transactivation function of HIF-1alpha by promoting dissociation of HIF-1alpha from FIH-1 and association with p300.
- HDAC4 contributes to transcriptional induction of mPGES-1 by IL-1 through a mechanism involving up-regulation of Egr-1 transcriptional activity