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Details on Person To carry out gene expression, a cell must control the windin...
| Class:Id | Summation:9685408 |
|---|---|
| _displayName | To carry out gene expression, a cell must control the windin... |
| _timestamp | 2021-05-28 14:01:38 |
| created | [InstanceEdit:9685409] Jassal, Bijay, 2020-04-23 |
| literatureReference | [LiteratureReference:9685416] Vorinostat, a pan-HDAC inhibitor, abrogates productive HPV-18 DNA amplification [LiteratureReference:9685411] Belinostat for Relapsed or Refractory Peripheral T-Cell Lymphoma [LiteratureReference:9685439] Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas |
| modified | [InstanceEdit:9691332] Jassal, Bijay, 2020-06-11 [InstanceEdit:9731772] Jassal, Bijay, 2021-05-24 [InstanceEdit:9732578] Jassal, Bijay, 2021-05-28 |
| text | To carry out gene expression, a cell must control the winding and unwinding of DNA around histones. This is mediated by histone acetyl transferases (HATs) and histone deacetylases (HDACs). HDAC inhibitors inhibit the proliferation of tumour cells by inducing cell cycle arrest, differentiation and/or apoptosis (Zhang et al. 2019). Belinostat (Marks et al. 2000, O'Connor et al. 2015), vorinostat (Marks & Breslow 2007) and romidepsin (Ueda et al. 1994, VanderMolen et al. 2011) are HDAC inhibitors approved for the treatment of Peripheral T-cell lymphomas (PTCLs) (Hood & Shah 2016). These drugs are believed to bind to many, if not all HDAC proteins. Human papillomaviruses (HPVs) cause epithelial proliferative diseases. The HDAC inhibitors vorinostat, belinostat and panobinostat have been shown to inhibit HPV DNA amplification and cause apoptosis in preclinical experiments (Banerjee et al. 2018). The antiepileptic drug valproic acid inhibits HDAC2 and therefore is a promising drug for cancer therapy (Göttlicher et al. 2001). |
| (summation) | [Reaction:9679787] HDAC1:2-containing complex binds HDAC2 Inhibitors [Homo sapiens] |
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