|1.||Lis, John T: 8 articles (02/2014 - 12/2002)|
|2.||Sandri-Goldin, Rozanne M: 4 articles (01/2013 - 04/2006)|
|3.||Sano, Motoaki: 4 articles (01/2012 - 03/2003)|
|4.||Shilatifard, Ali: 4 articles (12/2011 - 02/2005)|
|5.||Baas, Frank: 4 articles (12/2005 - 04/2002)|
|6.||Boyer, Thomas G: 3 articles (10/2015 - 11/2012)|
|7.||Abdellatif, Maha: 3 articles (01/2015 - 03/2012)|
|8.||Gilmour, David S: 3 articles (01/2015 - 06/2010)|
|9.||Sayed, Danish: 3 articles (01/2015 - 03/2012)|
|10.||Yang, Zhi: 3 articles (01/2015 - 03/2012)|
10/01/2014 - "Low inhibitor doses cause rapid clearance of paused RNA polymerase II (RNAPII) molecules and sufficed to cause genome-wide alterations in gene expression, delays in cell cycle progression at both the G1/S and G2/M checkpoints, and diminished survival of human tumor cells. "
10/15/2015 - "The human RNA polymerase II (RNAPII)-associated factor complex (hPAFc) and its individual subunits have been implicated in human diseases, including cancer. "
05/02/2014 - "While EAF2 and its partner ELL have been shown to be members of protein complexes involved in RNA polymerase II transcriptional elongation, the biologic roles for EAF2 especially with regards to the development of cancer remains poorly understood. "
01/10/2014 - "Consistent with its tumor suppressor role, CDC73 binds to RNA polymerase II as part of a PAF1 transcriptional regulatory complex and causes transcriptional repression of oncogenes MYC and CCND1. "
01/01/2014 - "At the molecular and cellular level, LDC000067 reproduced effects characteristic of CDK9 inhibition such as enhanced pausing of RNA polymerase II on genes and, most importantly, induction of apoptosis in cancer cells. "
01/01/2010 - "Knocking down p300 resulted in dramatic down-regulation of hypoxic stimulation of EPO gene transcription, negated recruitment of RNA polymerase II to the gene's promoter, and eliminated hypoxia-stimulated acetylation at the promoter and recruitments of SRC-1 and SRC-3 to the enhancer. "
04/03/2014 - "Genome-wide mapping of the XBP1 transcriptional regulatory network revealed that XBP1 drives TNBC tumorigenicity by assembling a transcriptional complex with HIF1α that regulates the expression of HIF1α targets via the recruitment of RNA polymerase II. Analysis of independent cohorts of patients with TNBC revealed a specific XBP1 gene expression signature that was highly correlated with HIF1α and hypoxia-driven signatures and that strongly associated with poor prognosis. "
04/22/2011 - "Repression of ESR1 gene transcription occurred at the transcriptional level as a result of decreased recruitment of RNA polymerase II at the proximal promoter of the ESR1 locus in response to stabilization of the HIF-1α protein under hypoxia. "
02/26/2010 - "Hypoxia-dependent induction of KAI1 was directly mediated by hypoxia-inducible factor (HIF)-1alpha binding on the promoter, which subsequently caused increased recruitment of RNA polymerase II for transcriptional activation. "
02/18/2009 - "Intermittent hypoxia regulates RNA polymerase II in hippocampus and prefrontal cortex."
09/01/2005 - "Previous studies have shown that herpes simplex virus type 1 (HSV-1) infection alters the phosphorylation of the carboxyl-terminal domain (CTD) of RNA polymerase II (RNAP II), creating a new form of the enzyme known as RNAP II(I). "
07/01/2015 - "Most subunits of the RNA polymerase II complex were progressively degraded, which likely contributes to the transcriptional host shut-off observed during CHIKV infection. "
10/01/2014 - "Depletion of 19S RP subunits generated a defect in RNA polymerase II elongation through the MIE locus during HCMV infection. "
06/01/2014 - "The results showed that before pathogen infection, mediator of RNA polymerase II transcription subunit 8 and β-actin were ranked as the most stable genes across the examined tissues. "
03/01/2014 - "Despite this fact, RNA polymerase II (RNAP II) is degraded during infection in a process triggered by the viral polymerase. "
|4.||Breast Neoplasms (Breast Cancer)
01/20/2015 - "Chip-on-chip with anti-RNA polymerase II was compared among breast cancer cell lines to identify genes that are potentially activated by HER2. "
01/01/2013 - "The recruited chromatin remodeling activity leads to the RNA polymerase II carboxy-terminal domain phosphorylation at the TFF1 promoter, initiating TFF1 expression in MCF-7 breast cancer cells. "
06/01/2012 - "pombe), O-6-methylguanine-DNA methyltransferase and RNA polymerase II-associated protein 1. The identified markers may be relevant to breast cancer susceptibility in populations if these findings are confirmed in independent cohorts."
01/01/2013 - "The aim of this study was to determine the correlation of γ-glutamyl hydrolase (GGH), fatty acid amide hydrolase (FAAH), Pirin (PIR) and TAF5-like RNA polymerase II, p300/CBP-associated factor (PCAF)-associated factor, 65 kDa (TAF5L), selected from identified gene signatures, with clinical outcomes as well as classical clinicopathological characteristics in primary invasive breast cancer patients. "
01/28/2011 - "In this study, we revealed that RPAP3 (RNA polymerase II-associated protein 3) possesses an activity to bind with NEMO and to inhibit the ubiquitination of NEMO and that RPAP3 enhances doxorubicin-induced cell death in breast cancer cell line T-47D through the marked impairment of NF-κB pathway. "
01/01/2015 - "Most of our studies employ the hsp70 heat shock gene promoter; however, this technique has successfully reconstituted RNA polymerase II pausing downstream of several other Drosophila promoters. "
09/01/2012 - "Fcp1 dephosphorylation of the RNA polymerase II C-terminal domain is required for efficient transcription of heat shock genes."
02/01/2012 - "The large noncoding hsrω-n transcripts are essential for thermotolerance and remobilization of hnRNPs, HP1 and RNA polymerase II during recovery from heat shock in Drosophila."
10/01/2010 - "Moreover, HP1c guides the recruitment of FACT to active genes and links FACT to active forms of RNA polymerase II. The absence of HP1c partially impairs the recruitment of FACT into heat-shock loci and causes a defect in heat-shock gene expression. "
02/01/2008 - "The recruitment of Gcn5 was Swi/Snf-dependent and was required for HSF (heat-shock factor) binding and affected RNAPII (RNA polymerase II) recruitment, whereas Elp3 exerted its roles mainly through affecting RNAPII elongation. "
|2.||DNA (Deoxyribonucleic Acid)
|3.||RNA (Ribonucleic Acid)
|4.||Proteins (Proteins, Gene)
|5.||DNA Polymerase II
|6.||DNA-Directed RNA Polymerases (RNA Polymerase)
|9.||Actins (F Actin)
|10.||Transcription Factors (Transcription Factor)
|1.||Heterologous Transplantation (Xenotransplantation)
|3.||Cardiopulmonary Resuscitation (CPR)
|4.||Transplantation (Transplant Recipients)
|5.||Tissue Therapy (Cell Therapy)