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https://www.readbyqxmd.com/read/29784880/arginine-methylation-of-translocated-in-liposarcoma-tls-inhibits-its-binding-to-long-noncoding-rna-abrogating-tls-mediated-repression-of-cbp-p300-activity
#1
Wei Cui, Ryoma Yoneda, Naomi Ueda, Riki Kurokawa
Translocated in liposarcoma (TLS) is an RNA-binding protein and a transcription-regulatory sensor of DNA damage. TLS binds promoter-associated noncoding RNA (pncRNA) and inhibits histone acetyltransferase (HAT) activity of CREB-binding protein (CBP)/E1A-binding protein P300 (p300) on the cyclin D1 (CCND1) gene. Although post-translational modifications of TLS, such as arginine methylation, are known to regulate TLS's nucleocytoplasmic shuttling and assembly in stress granules, its interactions with RNAs remain poorly characterized...
May 21, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29772755/temozolomide-enhances-triple-negative-breast-cancer-virotherapy-in-vitro
#2
Rodolfo Garza-Morales, Roxana Gonzalez-Ramos, Akiko Chiba, Roberto Montes de Oca-Luna, Lacey R McNally, Kelly M McMasters, Jorge G Gomez-Gutierrez
Triple-negative breast cancer (TNBC) is one of the most aggressive types of cancer, and treatment is limited to chemotherapy and radiation. Oncolytic virotherapy may be a promising approach to treat TNBC. However, oncolytic adenovirus (OAd)-based mono-therapeutic clinical trials have resulted in modest outcomes. The OAd potency could be increased by chemotherapy-induced autophagy, an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. In this study, the ability of alkylating agent temozolomide (TMZ)-induced autophagy to increase OAd replication and oncolysis in TNBC cells was evaluated...
May 17, 2018: Cancers
https://www.readbyqxmd.com/read/29743362/adenovirus-5-e1a-mediated-suppression-of-p53-via-fubp1
#3
Jasmine Rae Frost, Megan Mendez, Andrea Michelle Soriano, Leandro Crisostomo, Oladunni Olanubi, Sandi Radko, Peter Pelka
The Far Upstream Element Binding Protein 1 (FUBP1) was first identified as a regulator of the oncogene c-Myc via binding to the Far Upstream Element (FUSE) within the c-Myc promoter and activating expression of the gene. Recent studies have identified FUBP1 as a regulator of transcription, translation, and splicing via its DNA and RNA binding activities. Here we report the identification of FUBP1 as a novel binding partner of E1A. FUBP1 binds directly to E1A via the N-terminus (residues 1-82) and Conserved Region 3 (residues 139 to 204) of adenovirus 5 E1A...
May 9, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29717655/hypoxia-inducible-factor-1%C3%AE-hif-1%C3%AE-expression-on-endothelial-cells-in-juvenile-nasopharyngeal-angiofibroma-a-review-of-70-cases-and-tissue-microarray-analysis
#4
Xiaole Song, Chenhe Yang, Huankang Zhang, Jingjing Wang, Xicai Sun, Li Hu, Zhuofu Liu, Dehui Wang
OBJECTIVE: To examine the expression of hypoxia-inducible factor-1α (HIF-1α) and its related molecules (cellular repressor of E1A-stimulated genes [CREG], osteopontin [OPN], proto-oncogene tyrosine-protein kinase Src [c-Src], and vascular endothelial growth factor [VEGF]) in juvenile nasopharyngeal angiofibroma (JNA) and explore the correlation between clinical prognosis and HIF-1α expression. METHODS: The study performed a retrospective review of the clinical records of patients with JNA treated between 2003 and 2007...
April 1, 2018: Annals of Otology, Rhinology, and Laryngology
https://www.readbyqxmd.com/read/29717008/hacking-the-cell-network-intrusion-and-exploitation-by-adenovirus-e1a
#5
REVIEW
Cason R King, Ali Zhang, Tanner M Tessier, Steven F Gameiro, Joe S Mymryk
As obligate intracellular parasites, viruses are dependent on their infected hosts for survival. Consequently, viruses are under enormous selective pressure to utilize available cellular components and processes to their own advantage. As most, if not all, cellular activities are regulated at some level via protein interactions, host protein interaction networks are particularly vulnerable to viral exploitation. Indeed, viral proteins frequently target highly connected "hub" proteins to "hack" the cellular network, defining the molecular basis for viral control over the host...
May 1, 2018: MBio
https://www.readbyqxmd.com/read/29684345/transplantation-of-creg-modified-embryonic-stem-cells-improves-cardiac-function-after-myocardial-infarction-in-mice
#6
Jian Zhang, Xiaoxiang Tian, Chengfei Peng, Chenghui Yan, Yang Li, Mingyu Sun, Jian Kang, Erhe Gao, Yaling Han
Engraftment of embryonic stem cells (ESC) has been proposed as a potential therapeutic approach for post-infarction cardiac dysfunction. However, only mild function improvement has been achieved due to low survival rate and paracrine dysfunction of transplanted stem cells. Cellular repressor of E1A stimulated genes (CREG) has been reported to be a secreted glycoprotein implicated in promoting survival and differentiation of many cell types. Therefore we hypothesized that transplantation of genetically modified ESC with CREG (CREG-ESC) can improve cardiac function after myocardial infarction in mice...
April 20, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29593045/degradation-of-a-novel-dna-damage-response-protein-tankyrase-1-binding-protein-1-tab182-following-adenovirus-infection
#7
Nafiseh Chalabi Hagkarim, Ellis L Ryan, Philip J Byrd, Robert Hollingworth, Neil J Shimwell, Angelo Agathanggelou, Manon Vavasseur, Viktoria Kolbe, Thomas Speiseder, Thomas Dobner, Grant S Stewart, Roger J Grand
Infection by most DNA viruses activates a cellular DNA damage response (DDR), which may be to the detriment or advantage of the virus. In the case of adenoviruses, they neutralise anti-viral effects of DDR activation by targeting a number of proteins for rapid proteasome-mediated degradation. We have now identified a novel DDR protein, tankyrase 1 binding protein 1 (TNKS1BP1 also known as Tab182), which is degraded during infection by adenovirus 5 and adenovirus 12. In both cases, degradation requires the action of E1B55K and E4orf6 viral proteins and is mediated through the proteasome by the action of cullin-based cellular E3 ligases...
March 28, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29531323/pre-b-acute-lymphoblastic-leukaemia-recurrent-fusion-ep300-znf384-is-associated-with-a-distinct-gene-expression
#8
Barbara J McClure, Susan L Heatley, Chung H Kok, Teresa Sadras, Jiyuan An, Timothy P Hughes, Richard B Lock, David Yeung, Rosemary Sutton, Deborah L White
BACKGROUND: Zinc-finger protein 384 (ZNF384) fusions are an emerging subtype of precursor B-cell acute lymphoblastic leukaemia (pre-B-ALL) and here we further characterised their prevalence, survival outcomes and transcriptome. METHODS: Bone marrow mononuclear cells from 274 BCR-ABL1-negative pre-B-ALL patients were immunophenotyped and transcriptome molecularly characterised. Transcriptomic data was analysed by principal component analysis and gene-set enrichment analysis to identify gene and pathway expression changes...
April 2018: British Journal of Cancer
https://www.readbyqxmd.com/read/29480719/adenovirus-replication-cycle-disruption-from-exposure-to-polychromatic-ultraviolet-irradiation
#9
Bernardo Vazquez-Bravo, Kelley Gonçalves, Joanna L Shisler, Benito J Mariñas
Polychromatic ultraviolet (UV) light with bandwidth of 20 nm and peak emission centered at 224, 254, or 280 nm (UV224 , UV254 , and UV280 , respectively) were used to inactivate human adenovirus type 2 (HAdV-2). Quantitative polymerase chain reaction (qPCR) and reverse transcriptase qPCR assays were used to elucidate the step in the HAdV-2 replication cycle that was disrupted after UV exposure. UV treatment at any of the wavelengths analyzed did not inhibit association of HAdV-2 to the host cells even after exposure to a fluence (UV dose) that would produce a virus inactivation efficiency, measured by plaque assay, greater than 99...
March 20, 2018: Environmental Science & Technology
https://www.readbyqxmd.com/read/29454793/p300-acetyltransferase-mediates-stiffness-induced-activation-of-hepatic-stellate-cells-into-tumor-promoting-myofibroblasts
#10
Changwei Dou, Zhikui Liu, Kangsheng Tu, Hongbin Zhang, Chen Chen, Usman Yaqoob, Yuanguo Wang, Jialing Wen, Jan van Deursen, Delphine Sicard, Daniel Tschumperlin, Hongzhi Zou, Wei-Chien Huang, Raul Urrutia, Vijay H Shah, Ningling Kang
BACKGROUND & AIMS: Hepatic stellate cells (HSCs) contribute to desmoplasia and stiffness of liver metastases by differentiating into matrix-producing myofibroblasts. We investigated whether stiffness due to the presence of tumors increases activation of HSCs into myofibroblasts and their tumor-promoting effects, as well as the role of E1A binding protein p300 (EP300 or p300), a histone acetyltransferase that regulates transcription, in these processes. METHODS: HSCs were isolated from liver tissues of patients, mice in which the p300 gene was flanked by 2 loxP sites (p300F/F mice), and p300+/+ mice (controls)...
February 15, 2018: Gastroenterology
https://www.readbyqxmd.com/read/29444744/overexpression-of-pyruvate-dehydrogenase-e1a-subunit-inhibits-warburg-effect-and-induces-cell-apoptosis-through-mitochondria-mediated-pathway-in-hepatocellular-carcinoma
#11
Jihong Sun, Jingjing Li, Zhixian Guo, Lu Sun, Chenghui Juan, Yubing Zhou, Hongli Gu, Yan Yu, Qiuyue Hu, Quancheng' Kan, Zujiang Yu
Most cancers rely disproportionately on glycolysis for energy even in the presence of adequate oxygen supply, a condition known as "aerobic glycolysis", or the "Warburg effect". Pyruvate dehydrogenase E1a subunit (PDHA1) is one of main factors for metabolic switch from oxidative phosphorylation (OXPHOS) to aerobic glycolysis and has been suggested to be closely associated with tumorigenesis. Here we observed that PDHA1 protein was reduced in hepatocellular carcinoma (HCC) specimens by immunohistochemistry and western blot, which was significantly associated with poor overall survival...
February 14, 2018: Oncology Research
https://www.readbyqxmd.com/read/29438228/antitumor-effect-of-the-newcastle-disease-viral-hemagglutinin-neuraminidase-gene-is-expressed-through-an-oncolytic-adenovirus-effect-in-osteosarcoma-cells
#12
Shuang Chen, Qinggao Zhang, Duo Xu, Yiquan Li, Yuanyuan Fan, Wenjie Li, Xunzhe Yin, Yang Zhang, Jingwei Liu, Xiao Li, Lili Sun, Ningyi Jin
Newcastle disease virus (NDV) can specifically kill cancer cells and has less toxicity to normal cells. The hemagglutinin-neuraminidase (HN) protein is an important structural protein in NDV pathogenesis and has been postulated as a promising candidate for antitumor therapy. The aim of this study was to investigate the anticancer potential of recombinant adenovirus Ad-HN-PEG3p-E1a. An MTS assay was performed to determine viral proliferation after viral infection, the data showed that the proliferation ability of osteosarcoma cells decreased, whereas there was no significant change in normal hepatic cells...
March 2018: Anti-cancer Drugs
https://www.readbyqxmd.com/read/29435080/a-novel-approach-to-glioma-therapy-using-an-oncolytic-adenovirus-with-two-specific-promoters
#13
Feng Liu, Kaya Xu, Hua Yang, Yuming Li, Jian Liu, Jixiang Wang, Zhizhong Guan
Gliomas are the most common type of primary brain tumor in adults, where more than half of the cases are malignant, and the prognosis is poor. The early viral 1A (E1A) protein has been widely recognized to be essential for adenoviral replication and production of progeny virions in human cells, a process that is regulated by human telomerase reverse transcriptase. The p53 gene, as a tumor suppressor, regulates diverse cellular processes, including cell cycle arrest, cell autophagy, senescence and apoptosis...
March 2018: Oncology Letters
https://www.readbyqxmd.com/read/29388837/adenovirus-lacking-e1b-efficiently-induces-cytopathic-effect-in-hpv-16-positive-murine-cancer-cells-via-virus-replication-and-apoptosis
#14
Elvis Martinez-Jaramillo, Rodolfo Garza-Morales, Stephen L Wechman, Roberto Montes de Oca-Luna, Odila Saucedo-Cardenas, Haval Shirwan, Esma Yolcu, Kelly M McMasters, Jorge G Gomez-Gutierrez
Conditionally replicative adenoviruses (CRAds) replicate poorly in murine cancer cells; however, E1b-deleted CRAds may replicate effectively in HPV16-E6/E7-positive murine cancer cells (TC-1). The HPV16 E7 open reading frame encodes functions analogous to these deleted adenovirus E1 proteins. In this study, an E1b-deleted CRAd (Adhz60) was evaluated for its ability to replicate and induce oncolysis in TC-1 cells. Adhz60-mediated oncolysis was similar in TC-1 and HeLa cells. Productive viral replication was evident based on expression of E1A and hexon, production of infectious virus progeny, and Adhz60-induced apoptosis...
January 2, 2018: Cancer Investigation
https://www.readbyqxmd.com/read/29367252/mimicry-of-cellular-a-kinase-anchoring-proteins-is-a-conserved-and-critical-function-of-e1a-across-various-human-adenovirus-species
#15
Cason R King, Steven F Gameiro, Tanner M Tessier, Ali Zhang, Joe S Mymryk
The E1A proteins of the various human adenovirus (HAdV) species perform the critical task of converting an infected cell into a setting primed for virus replication. While E1A proteins differ in both sequence and mechanism, the evolutionary pressure on viruses with limited coding capacity ensures that these proteins often have significant overlap in critical functions. HAdV-5 E1A is known to use mimicry to rewire cyclic AMP (cAMP) signaling by decoupling protein kinase A (PKA) from cellular A-kinase anchoring proteins (AKAPs) and utilizing PKA to its own advantage...
January 24, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29321817/enhanced-myc-association-with-the-nua4-histone-acetyltransferase-complex-mediated-by-the-adenovirus-e1a-n-terminal-domain-activates-a-subset-of-myc-target-genes-highly-expressed-in-cancer-cells
#16
Ling-Jun Zhao, Paul M Loewenstein, Maurice Green
The proto-oncogene MYC is a transcription factor over-expressed in many cancers and required for cell survival. Its function is regulated by histone acetyltransferase (HAT) complexes, such as the GCN5 complex and the NuA4/Tip60 complex. However, the roles of the HAT complexes during MYC function in cancer have not been well characterized. We recently showed that adenovirus E1A and its N-terminal 80 aa region, E1A 1-80, interact with the NuA4 complex, through the E1A TRRAP-targeting (ET) domain, and enhance MYC association with the NuA4 complex...
November 2017: Genes & Cancer
https://www.readbyqxmd.com/read/29241042/the-adenovirus-e1a-c-terminus-suppresses-a-delayed-antiviral-response-and-modulates-ras-signaling
#17
Nathan R Zemke, Arnold J Berk
The N-terminal half of adenovirus e1a assembles multimeric complexes with host proteins that repress innate immune responses and force host cells into S-phase. In contrast, the functions of e1a's C-terminal interactions with FOXK, DCAF7, and CtBP are unknown. We found that these interactions modulate RAS signaling, and that a single e1a molecule must bind all three of these host proteins to suppress activation of a subset of IFN-stimulated genes (ISGs). These ISGs were otherwise induced in primary respiratory epithelial cells at 12 hr p...
December 13, 2017: Cell Host & Microbe
https://www.readbyqxmd.com/read/29238045/ripk3-promotes-adenovirus-type-5-activity
#18
Melanie Weigert, Alex Binks, Suzanne Dowson, Elaine Y L Leung, Dimitris Athineos, Xinzi Yu, Margaret Mullin, Josephine B Walton, Clare Orange, Darren Ennis, Karen Blyth, Stephen W G Tait, Iain A McNeish
Oncolytic adenoviral mutants infect human malignant cells and replicate selectively within them. This induces direct cytotoxicity that can also trigger profound innate and adaptive immune responses. However, the mechanism by which adenoviruses produce cell death remains uncertain. We previously suggested that type 5 adenoviruses, including the E1A CR2 deletion mutant dl922-947, might induce a novel form of programmed death resembling necroptosis. Here we have investigated the roles of core necrosis proteins RIPK1, RIPK3 and MLKL in the cytotoxicity of dl922-947 and other adenovirus serotypes...
December 13, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/29228615/combined-therapy-of-colon-carcinomas-with-an-oncolytic-adenovirus-and-valproic-acid
#19
Christian Bressy, Dragomira Majhen, Najat Raddi, Wael Jdey, Gaétan Cornilleau, Léna Zig, Josée Guirouilh-Barbat, Bernard S Lopez, Olivia Bawa, Paule Opolon, Elodie Grellier, Karim Benihoud
The anti-tumor potential of oncolytic adenoviruses (CRAds) has been demonstrated in preclinical and clinical studies. While these agents failed to eradicate tumors when used as a monotherapy, they may be more effective if combined with conventional treatments such as radiotherapy or chemotherapy. This study seeks to evaluate the combination of a CRAd bearing a ∆24 deletion in E1A with valproic acid (VPA), a histone deacetylase inhibitor, for the treatment of human colon carcinomas. This combination led to a strong inhibition of cell growth both in vitro and in vivo compared to treatment with CRAd or VPA alone...
November 14, 2017: Oncotarget
https://www.readbyqxmd.com/read/29163768/inhibitor-of-growth-protein-4-interacts-with-beclin-1-and-represses-autophagy
#20
Valentina Sica, José Manuel Bravo-San Pedro, Guo Chen, Guillermo Mariño, Sylvie Lachkar, Valentina Izzo, Maria Chiara Maiuri, Mireia Niso-Santano, Guido Kroemer
Beclin 1 (BECN1) is a multifunctional protein that activates the pro-autophagic class III phosphatidylinositol 3-kinase (PIK3C3, best known as VPS34), yet also interacts with multiple negative regulators. Here we report that BECN1 interacts with inhibitor of growth family member 4 (ING4), a tumor suppressor protein that is best known for its capacity to interact with the tumor suppressor protein p53 (TP53) and the acetyltransferase E1A binding protein p300 (EP300). Removal of TP53 or EP300 did not affect the BECN1/ING4 interaction, which however was lost upon culture of cells in autophagy-inducing, nutrient free conditions...
October 27, 2017: Oncotarget
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