scholarly journals Gene Expression Mapping of Histone Deacetylases and Co-factors and Correlation with Survival Time and 1H-HRMAS Metabolomic Profile in Human Gliomas

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Nassim Dali-Youcef ◽  
Sébastien Froelich ◽  
François-Marie Moussallieh ◽  
Salvatore Chibbaro ◽  
Georges Noël ◽  
...  

2020 ◽  
Vol 495 (1) ◽  
pp. 338-341
Author(s):  
Yu. V. Gritsyna ◽  
A. D. Ulanova ◽  
S. S. Popova ◽  
A. G. Bobylev ◽  
V. K. Zhalimov ◽  
...  


2006 ◽  
Vol 70 (6) ◽  
pp. 1876-1884 ◽  
Author(s):  
Giuseppe Faraco ◽  
Tristano Pancani ◽  
Laura Formentini ◽  
Paolo Mascagni ◽  
Gianluca Fossati ◽  
...  


2001 ◽  
Vol 18 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Atsushi Sasaki ◽  
Shogo Ishiuchi ◽  
Tsugiyasu Kanda ◽  
Masatoshi Hasegawa ◽  
Yoichi Nakazato


2015 ◽  
Vol 9 ◽  
Author(s):  
Okamura-Oho Yuko ◽  
Morita Masahiko ◽  
Shimokawa Kazuro ◽  
Nishimura Masaomi ◽  
Tawara Takehiro ◽  
...  


2019 ◽  
Author(s):  
Sina Dalvand ◽  
Amin Namdari ◽  
Ashraf Alemi ◽  
Mohammad Hassan Meshkibaf ◽  
Sam Setayesh ◽  
...  

Abstract Background: Histone modifications play a crucial role in chromatin structure. Among enzymes, which regulate these processes, histone deacetylases (HDACs) can remove acetyl groups from histone tails, thus increasing their interaction with DNA and leading to chromatin condensation. 5-Aza-2′-deoxycytidine (AZad) or Decitabine is a potent hypomethylating agent that incorporates into DNA and traps DNA methyltransferase in the form of a covalent protein–DNA adduct. Azad, not only change the gene expression through demethylation of the gene's promoter, but it also can change gene expression independently from DNA demethylation. So, the present study was to distinguish whether AZad in addition to inhibitory effects on DNA methyltransferase, can change HDAC3 and HDAC7 mRNA expression in NALM-6, HL-60 cancer cell lines. Methods: HL-60, NALM-6 and normal cells were cultured, and the treatment dose of the AZad was obtained (1µM) by the MTT test. Finally, HDAC3 and HDAC7 mRNA expression were measured by Real Time PCR in HL-60 and NALM-6 cancerous cells before and after treatment. In addition, HDAC3 and HDAC7 mRNA expression in un-treated HL-60 and NALM-6 cancerous cells were compared to the normal cells. Results: Our result revealed that expression of HDAC3 and HDAC7, in HL-60 and NALM-6 cells increases as compared to normal cells. After treatment of HL-60 and NALM-6 cells with AZad, HDAC3 and HDAC7 mRNA expression were decreased significantly. Conclusions: Our data showed, the effects of AZad are not limited to direct hypomethylation of DNMTs but it can indirectly affect other epigenetic factors, such as HDACs activity, through converging pathways. Keywords: HDAC3 ; HDAC7 ; HL-60; NALM-6 ; Decitabine ; AZad





Author(s):  
Edward Hookway ◽  
Nicholas Athanasou ◽  
Udo Oppermann

Epigenetics is a term that refers to a collection of diverse mechanisms that are important in both the control of gene expression and the transmission of this information during cell division. Epigenetic processes are deranged in many cancers, leading to a combination of inappropriate silencing of tumour suppressor genes and overexpression of oncogenes. In this chapter, the molecular mechanisms that underpin the major epigenetic processes of DNA methylation, histone modification, and non-coding RNAs will be described in both their normal physiological roles and in the context of cancer. The challenge of understanding the complexity of the interactions between different epigenetic mechanisms and the limitations of our current knowledge will be highlighted. Therapeutic approaches towards targeting deranged epigenetic processes will also be described, such as the use of small molecule inhibitors of histone deacetylases.



Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1120 ◽  
Author(s):  
Levi Evans ◽  
Bradley Ferguson

Approximately 5.7 million U.S. adults have been diagnosed with heart failure (HF). More concerning is that one in nine U.S. deaths included HF as a contributing cause. Current HF drugs (e.g., β-blockers, ACEi) target intracellular signaling cascades downstream of cell surface receptors to prevent cardiac pump dysfunction. However, these drugs fail to target other redundant intracellular signaling pathways and, therefore, limit drug efficacy. As such, it has been postulated that compounds designed to target shared downstream mediators of these signaling pathways would be more efficacious for the treatment of HF. Histone deacetylation has been linked as a key pathogenetic element for the development of HF. Lysine residues undergo diverse and reversible post-translational modifications that include acetylation and have historically been studied as epigenetic modifiers of histone tails within chromatin that provide an important mechanism for regulating gene expression. Of recent, bioactive compounds within our diet have been linked to the regulation of gene expression, in part, through regulation of the epi-genome. It has been reported that food bioactives regulate histone acetylation via direct regulation of writer (histone acetyl transferases, HATs) and eraser (histone deacetylases, HDACs) proteins. Therefore, bioactive food compounds offer unique therapeutic strategies as epigenetic modifiers of heart failure. This review will highlight food bio-actives as modifiers of histone deacetylase activity in the heart.



2009 ◽  
Vol 106 (32) ◽  
pp. 13365-13370 ◽  
Author(s):  
M. Distel ◽  
M. F. Wullimann ◽  
R. W. Koster


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