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Validated All-in-One™ qPCR Primer for HDAC1(NM_004964.2) Search again
Product ID:
HQP008745
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GON-10, HD1, KDAC1, RPD3, RPD3L1
Gene Description:
histone deacetylase 1
Target Gene Accession:
NM_004964.2(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
Histone acetylation and deacetylation, catalyzed by multisubunit complexes, play a key role in the regulation of eukaryotic gene expression. The protein encoded by this gene belongs to the histone deacetylase/acuc/apha family and is a component of the histone deacetylase complex. It also interacts with retinoblastoma tumor-suppressor protein and this complex is a key element in the control of cell proliferation and differentiation. Together with metastasis-associated protein-2, it deacetylates p53 and modulates its effect on cell growth and apoptosis. [provided by RefSeq].
Gene References into function
- The transcriptional repressor mSin3A associates with histone deacetylase 1 forming a co-repressor complex. See also PMID (PubMed identifier) 9150133.
- Expression profile of histone deacetylase 1 in gastric cancer tissues
- role in regulation of the telomerase reverse transcriptase (hTERT) gene
- Phosphatase inhibition leads to histone deacetylases 1 and 2 phosphorylation and disruption of corepressor interactions
- association with proliferating cell nuclar antigen, integrating DNA replication and chromatin modification
- Counterregulation of chromatin deacetylation and histone deacetylase occupancy at the integrated promoter of human immunodeficiency virus type 1 (HIV-1) by the HIV-1 repressor YY1 and HIV-1 activator Tat.
- Androgen receptor, Tip60, and HDAC1 form a trimeric complex upon the endogenous AR-responsive PSA promoter, acetylation and deacetylation of the AR is an important mechanism for regulating transcriptional activity.
- interaction with large subunit of replication factor C
- associated with silencing DAP kinase gene expression in colorectal and gastric cancers
- HDAC-Sin3A complex regulates LHR Gene transcription
- interaction with mCpG-binding domain of MBD2
- localization in Aurora-A-positive centrosomes in M phase
- Data show that the adenovirus protein Gam1 counteracts histone deacetylase 1 sumoylation both in vivo and in vitro.
- The HDAC1 complex binds MDM2 in a p53-independent manner and deacetylates p53 at all known acetylated lysines in vivo.
- Che-1 affects cell growth by interfering with the recruitment of HDAC1 by retinoblastoma protein. Che-1 overexpression activates DNA synthesis in quiescent NIH-3T3 cells through HDAC1 displacement.
- recruited by prohibitin for transcriptional repression
- We demonstrate that MI-ER1 repressor activity is due to interaction and recruitment of a trichostatin A-sensitive HDAC1, deletion analysis revealed that recruitment of HDAC1 to hMI-ER1alpha and hMI-ER1beta occurs through their common ELM2 domain.
- Here we show that HDAC1 associates with and blocks Ser133 phosphorylation of CREB during pre-stimulus and attenuation phases of the cAMP response
- histone deacetylase 1 overexpression is associated with advanced stage esophageal squamous cell carcinoma.
- deacetylase HDAC1 acts as an antagonist of the tumor suppressor p53 in the regulation of the cyclin-dependent kinase inhibitor p21
- We investigated occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between pRb2/p130 and chromatin-modifying enzymes in the regulation of ER-alpha transcription
- p52 NF-kappaB subunit associates with histone deacetylase 1 when p53 represses cyclin D1 transcription through down regulation of Bcl-3
- The MLL repression domain specifically interacts with HDAC1.
- HDAC1 is displaced from the p21WAF1/CIP1 promoter by Che-1 in human colonic carcinoma
- IkappaBalpha regulates the transcriptional activity of homeodomain-containing proteins positively through cytoplasmic sequestration of HDAC1 and HDAC3
- HDAC1 represses the small GTPase RhoB expression in human nonsmall lung carcinoma cell line.
- HDAC1 has a role in interferon-stimulated transcription and innate antiviral immunity
- MeCP2 acts as a corepressor of PU.1 probably due to facilitating complex formation with mSin3A and HDACs.
- HDAC1 interacts with p300 C/H3 domain. Its overexpression interferes with either activation of Gal14p300 fusion protein or p300-dependent co-activation of MyoD and p53. E1A competes with HDAC1 for C/H3 binding.
- interaction of HPV type 31 E7 with HDACs and the integrity of the zinc finger-like motifs are essential for extending the life span of keratinocytes and for stable maintenance of viral genomes
- HDAC1 upregulated in pre-malignant and malignant lesions, with the highest increase in expression in hormone refractory (HR) prostate cancer; in CWR22 xenograft model, androgen dependent regulation of HDAC1 demonstrated.
- Ezh2 competes with HDAC1 in binding to pRb2/p130, disrupting their occupancy on the cyclin A promoter.
- histone deacetylase has a role in transforming growth factor-beta signaling in breast cancer cells
- Tax interacts directly with HDAC1 and regulates binding of the repressor to the HTLV-1 promoter
- SENP1's ability to enhance AR-dependent transcription is not mediated through desumoylation of AR, but rather through its ability to deconjugate histone deacetylase 1 (HDAC1), thereby reducing its deacetylase activity.
- stabilization of NF-E4 by acetylation is PCAF-dependent; acetylation of Lys(43) also reduces the interaction between NF-E4 and HDAC1, potentially maximizing the activating ability of the factor
- Accumulation of ICBP90 in breast-cancer cells might suppress expression of tumor suppressor genes through deacetylation of histones after recruitment of HDAC1.
- In prostate tissues, the abundance of HDAC1 protein, which was exclusively expressed in the cell nucleus, was similar in normal and malignant epithelial cells, but was usually lower in stromal cells.
- HDAC1 negatively regulates the cardiovascular transcription factor KLF5 through direct interaction
- plays a critical role in repression of endothelial constitutive nitric oxide synthase gene
- interleukin-5 transcription repression by the glucocorticoid receptor targets GATA3 signaling and involves histone deacetylase recruitment
- SMAR1 regulates cyclin D1 by modification of chromatin through the SIN3/histone deacetylase 1 complex
- HDAC1 mRNA expression could have potential as an endocrine response marker and may have prognostic implications for breast cancer progression
- Gfi1 associates with G9a and HDAC1 on the promoter of the cell cycle regulator p21Cip/WAF1, resulting in an increase in K9 dimethylation at histone H3
- NF-kappaB p50-HDAC1 complexes constitutively bind the latent HIV LTR and induce histone deacetylation and repressive changes in chromatin structure of the HIV LTR, changes that impair recruitment of RNA polymerase II and transcriptional initiation.
- Data suggest that the activation of programmes of gene expression by pro-inflammatory agents requires global changes in specific critical epigenetic regulators such as histone deacetylase 1.
- HER-2/neu induces the binding of Sp proteins and HDAC1 to the RECK promoter to inhibit RECK expression and to promote cell invasion
- apicidin activation of NF-kappaB seems to result from HDAC1 inhibition, as evidenced by the observation that overexpression of HDAC1, but not HDAC2, 3 or 4, dramatically inhibits NF-kappaB reporter gene activity.
- These studies reveal an intimate link between the histone demethylase and deacetylase enzymes but also identify histone demethylation as a secondary target of Histone deacetylase (HDAC) inhibitors.
- Human PIRH2 as a key modulator of AR function, opening a new direction for targeted therapy in aggressive human prostate cancer.
- study demonstrated that expression of DNMT1 is clearly regulated in both impaired spermatogenesis and development of embryonal carcinoma, while HDAC1 expression is not regulated during aberrant germ cell differentiation
- results show human cytomegalovirus IE86 interacts with HDAC1 and histone methyltransferases G9a and Suvar(3-9)H1 and that coexpression of these chromatin remodeling enzymes with IE86 increases autorepression of the major immediate-early promoter
- proteolysis studies suggest that HDAC1 comprises inter-related structural regions
- CREMalpha exerts its repressor activity by a mechanism that involves recruitment of HDAC1, increased deacetylation of histones, and repression of promoter activity.
- Our results suggest that HMTase WHISTLE induces apoptosis in an HMTase activity-dependent manner and represses transcription of target genes through HDAC1 recruitment.
- SUMO modification of the DEAD box protein p68 modulates its transcriptional activity and promotes its interaction with HDAC1
- Data suggest that MAT1-mediated transcriptional repressor (MMTR) is part of the basic cellular machinery for a wide range of transcriptional regulation via interaction with TFIIH and HDAC1.
- Results show for the first time acetylation via selective degradation of histone deacetylase 1, and that recruitment of histone acetyltransferase plays an important role in diesel exhaust particulate matter-induced expression of the cyclooxygenase-2 gene
- In the absence of HDAC1 cells can arrest either at the G(1) phase of the cell cycle or at the G(2)/M transition, resulting in the loss of mitotic cells, cell growth inhibition, and an increase in the percentage of apoptotic cells.
- Data show that increased generation of C18-ceramide by hCerS1 expression mediates the association and recruitment of deacetylated Sp3/HDAC1 to the hTERT promoter, resulting in local histone H3 deacetylation and repression of the promoter.
- all of the pathogenic HR mutants bound VDR but exhibited reduced binding to histone deacetylase 1 (HDAC1), suggesting that the impaired corepressor activity is due in part to defective interactions with HDACs
- ZBP-89 functions as a repressor by recruiting HDAC1 to the vimentin promoter.
- Myc, Sp1, and HDAC1 coexist in the same DNA-protein complex at the HIV promoter. Short hairpin RNA inhibition of c-Myc reduces both c-Myc and HDAC1 occupancy, blocks c-Myc repression of Tat activation, and increases LTR expression.
- High expression of HDAC1 is associated with cancer tissues
- HDAC1 has a role in melanoma cell senescence [news]
- PBF binds to SAP30 and represses transcription via recruitment of the HDAC1 co-repressor complex
- that interactions between C/EBPs and HDAC1 negatively regulate C/EBPdelta-dependent haptoglobin expression in intestinal epithelial cells.
- HDAC1 knockdown by small interference RNA stimulated uPA expression and cancer cell invasion.
- CK2 may be a key mediator for HDAC1 and HDAC2 activation under hypoxia in tumor cells
- The mRNA expression level of an epigenetically regulated schizophrenia candidate gene GAD67 was strongly and negatively correlated with the mRNA expression levels of HDAC1, HDAC3 and HDAC4 levels.
- Rev-erbbeta modulates the apoCIII gene expression by recruiting different transcription co-activator or co-repressor.
- High HDAC1 expression might have an important role in the aggressiveness and cell dedifferentiation in hepatocellular carcinoma
- ternary complex consisting of PPARdelta, p65/RelA, and HDAC1 in keratinocytes PPARdelta repression
- TRAF6 is modified by small ubiquitin-related modifier-1, interacts with histone deacetylase 1, and represses c-Myb-mediated transactivation.
- we showed that the known effects of HDACs on differentiation and proliferation of cancer cells observed in vitro can also be confirmed in vivo.
- These results demonstrate that HDAC1 could play a role in autophagy and specific inhibition of HDAC1 can induce autophagy.
- Strong prognostic impact of HDAC isoforms in colorectal cancer.
- HIF-1alpha expression may be regulated through HDAC1/MTA1, which is associated with a poor prognosis for pancreatic carcinoma
- A novel regulatory signaling mechanism of transcriptional control in which the LHR is derepressed through PKCalpha/ERK-mediated Sp1 phosphorylation, causing the release of HDAC1/mSin3A complex from the promoter.
- LPA enhances survival of cancer cells by increasing HDAC1 and HDAC2 activity and reducing histone acetylation
- The association between alphaB-crystallin and HDAC1 on SC35 speckles plays a pivotal role in anti-apoptotic activity.
- These results indicate that the hypoxia-induced activation of the XB-S promoter is regulated through dissociation of HDAC1 from an Sp1-binding hypoxia-responsive element site.
- Zac1 might be involved in regulating the p21(WAF1/Cip1) gene and protein expression through its protein-protein interaction with p53 and HDAC1 in HeLa cells.
- The immunohistochemical expression of HDAC1 in cutaneous T-cell lymphoma.
- Recruitment of HDAC-1 and -2 by TNF-alpha, and a consequent deacetylation of histone H3 at the YKL-40 promoter occurs only in glioma cells.
- class I HDACs suggest that these targets should be explored as predictive factors in ovarian and endometrial carcinomas prospectively.
- Different from ERbeta, p53 interacts with HDAC1 and CtBP1 and forms an inhibiting transcriptional complex that could compete for binding to Sp1 sites with ERalpha transcriptional complex and inhibit BRCA2 transcription more significantly
- Studies show that cancer cells effectively maintain low levels of pyruvate to prevent inhibition of HDAC1/HDAC3 and thereby to evade cell death.
- ZNF198, through its multiple protein-protein interaction interfaces, helps to maintain the intact LSD1-CoREST-HDAC1 complex on specific, non-REST-responsive promoters and may also prevent SUMO-dependent dissociation of HDAC1
- P/CAF deacetylation by HDAC3 and in a minor degree by HDAC1, HDAC2, or HDAC4 leads to cytoplasmic accumulation of P/CAF.