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https://www.readbyqxmd.com/read/27924510/global-protein-expression-analysis-of-molecular-markers-of-ds-1-47-a-component-of-implantation-promoting-traditional-chinese-medicine
#1
Yan-Ling Li, Xiao-Yan Zhang, Yu Leng, Yan-Li Wu, Jing Li, Yun-Xia Wu
This study investigated the molecular markers of DS-1-47, a component of an implantation- promoting traditional Chinese medicine consisting of Astragalus mongholicus, Atractylodes macrocephala, Scutellaria baicalensis and Dipsacales, in an attempt to clarify the molecular mechanism and action targets of DS-1-47. Controlled ovarian stimulation (COS) method was used to establish the implantation dysfunction models of mice. Animals were divided into normal pregnant group, COS model group and DS-1-47 group. Laser capture microdissection-double dimensional electrophoresis-mass spectrum (LCM-DE-MS) was used to analyze the uterine protein molecules that were possibly involved in the promotion of implantation...
December 2016: Journal of Huazhong University of Science and Technology. Medical Sciences
https://www.readbyqxmd.com/read/27923066/somatic-genomics-and-clinical-features-of-lung-adenocarcinoma-a-retrospective-study
#2
Jianxin Shi, Xing Hua, Bin Zhu, Sarangan Ravichandran, Mingyi Wang, Cu Nguyen, Seth A Brodie, Alessandro Palleschi, Marco Alloisio, Gianluca Pariscenti, Kristine Jones, Weiyin Zhou, Aaron J Bouk, Joseph Boland, Belynda Hicks, Adam Risch, Hunter Bennett, Brian T Luke, Lei Song, Jubao Duan, Pengyuan Liu, Takashi Kohno, Qingrong Chen, Daoud Meerzaman, Crystal Marconett, Ite Laird-Offringa, Ian Mills, Neil E Caporaso, Mitchell H Gail, Angela C Pesatori, Dario Consonni, Pier Alberto Bertazzi, Stephen J Chanock, Maria Teresa Landi
BACKGROUND: Lung adenocarcinoma (LUAD) is the most common histologic subtype of lung cancer and has a high risk of distant metastasis at every disease stage. We aimed to characterize the genomic landscape of LUAD and identify mutation signatures associated with tumor progression. METHODS AND FINDINGS: We performed an integrative genomic analysis, incorporating whole exome sequencing (WES), determination of DNA copy number and DNA methylation, and transcriptome sequencing for 101 LUAD samples from the Environment And Genetics in Lung cancer Etiology (EAGLE) study...
December 2016: PLoS Medicine
https://www.readbyqxmd.com/read/27890786/heat-increases-the-editing-efficiency-of-human-papillomavirus-e2-gene-by-inducing-upregulation-of-apobec3a-and-3g
#3
Yang Yang, Hexiao Wang, Xinrui Zhang, Wei Huo, Ruiqun Qi, Yali Gao, Gaofeng Zhang, Bing Song, Hongduo Chen, Xinghua Gao
Apolipoprotein B mRNA-editing catalytic polypeptide (APOBEC) 3 proteins have been identified as potent viral DNA mutators and have broad antiviral activity. In this study, we demonstrated APOBEC3A (A3A) and A3G expression levels were significantly upregulated in HPV infected cell lines and tissues. Heat treatment resulted in elevated expression of A3A and A3G in a temperature-dependent manner in HPV infected cells. Correspondingly, 44 ºC heating treated HPV infected cells showed accumulated G-to-A or C-to-T mutation in HPVE2 gene...
November 24, 2016: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/27869537/rna-binding-to-apobec-deaminases-not-simply-a-substrate-for-c-to-u-editing
#4
Harold C Smith
Apolipoprotein B mRNA Editing Catalytic Polypeptide-like 1 or APOBEC1 was discovered in 1993 as the zinc-dependent cytidine deaminase responsible for the production of an in frame stop codon in apoB mRNA through modification of cytidine at nucleotide position 6666 to uridine. At the time of this discovery there was much speculation concerning the mechanism of base modification RNA editing which has been rekindled by the discovery of multiple C to U RNA editing events in the 3' UTRs of mRNAs and the finding that other members of the APOBEC family while able to bind RNA, have the biological function of being DNA mutating enzymes...
November 21, 2016: RNA Biology
https://www.readbyqxmd.com/read/27815903/analysis-of-nuclear-uracil-dna-glycosylase-nudg-turnover-during-the-cell-cycle
#5
Jennifer A Fischer, Salvatore J Caradonna
Uracil-DNA glycosylases (UDG/UNG) are enzymes that remove uracil from DNA and initiate base-excision repair. These enzymes play a key role in maintaining genomic integrity by reducing the mutagenic events caused by G:C to A:T transition mutations. The recent finding that a family of RNA editing enzymes (AID/APOBECs) can deaminate cytosine in DNA has raised the interest in these base-excision repair enzymes. The methodology presented here focuses on determining the regulation of the nuclear isoform of uracil-DNA glycosylase (nUDG), a 36,000 Da protein...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27811275/mutational-signatures-associated-with-tobacco-smoking-in-human-cancer
#6
Ludmil B Alexandrov, Young Seok Ju, Kerstin Haase, Peter Van Loo, Iñigo Martincorena, Serena Nik-Zainal, Yasushi Totoki, Akihiro Fujimoto, Hidewaki Nakagawa, Tatsuhiro Shibata, Peter J Campbell, Paolo Vineis, David H Phillips, Michael R Stratton
Tobacco smoking increases the risk of at least 17 classes of human cancer. We analyzed somatic mutations and DNA methylation in 5243 cancers of types for which tobacco smoking confers an elevated risk. Smoking is associated with increased mutation burdens of multiple distinct mutational signatures, which contribute to different extents in different cancers. One of these signatures, mainly found in cancers derived from tissues directly exposed to tobacco smoke, is attributable to misreplication of DNA damage caused by tobacco carcinogens...
November 4, 2016: Science
https://www.readbyqxmd.com/read/27749842/clonal-evolution-of-chemotherapy-resistant-urothelial-carcinoma
#7
Bishoy M Faltas, Davide Prandi, Scott T Tagawa, Ana M Molina, David M Nanus, Cora Sternberg, Jonathan Rosenberg, Juan Miguel Mosquera, Brian Robinson, Olivier Elemento, Andrea Sboner, Himisha Beltran, Francesca Demichelis, Mark A Rubin
Chemotherapy-resistant urothelial carcinoma has no uniformly curative therapy. Understanding how selective pressure from chemotherapy directs the evolution of urothelial carcinoma and shapes its clonal architecture is a central biological question with clinical implications. To address this question, we performed whole-exome sequencing and clonality analysis of 72 urothelial carcinoma samples, including 16 matched sets of primary and advanced tumors prospectively collected before and after chemotherapy. Our analysis provided several insights: (i) chemotherapy-treated urothelial carcinoma is characterized by intra-patient mutational heterogeneity, and the majority of mutations are not shared; (ii) both branching evolution and metastatic spread are very early events in the natural history of urothelial carcinoma; (iii) chemotherapy-treated urothelial carcinoma is enriched with clonal mutations involving L1 cell adhesion molecule (L1CAM) and integrin signaling pathways; and (iv) APOBEC-induced mutagenesis is clonally enriched in chemotherapy-treated urothelial carcinoma and continues to shape the evolution of urothelial carcinoma throughout its lifetime...
December 2016: Nature Genetics
https://www.readbyqxmd.com/read/27734031/subtyping-sub-saharan-esophageal-squamous-cell-carcinoma-by-comprehensive-molecular-analysis
#8
Wenjin Liu, Jeff M Snell, William R Jeck, Katherine A Hoadley, Matthew D Wilkerson, Joel S Parker, Nirali Patel, Yohannie B Mlombe, Gift Mulima, N George Liomba, Lindsey L Wolf, Carol G Shores, Satish Gopal, Norman E Sharpless
Esophageal squamous cell carcinoma (ESCC) is endemic in regions of sub-Saharan Africa (SSA), where it is the third most common cancer. Here, we describe whole-exome tumor/normal sequencing and RNA transcriptomic analysis of 59 patients with ESCC in Malawi. We observed similar genetic aberrations as reported in Asian and North American cohorts, including mutations of TP53, CDKN2A, NFE2L2, CHEK2, NOTCH1, FAT1, and FBXW7. Analyses for nonhuman sequences did not reveal evidence for infection with HPV or other occult pathogens...
October 6, 2016: JCI Insight
https://www.readbyqxmd.com/read/27725676/genetics-apobec-conundrum-solved
#9
Lisa Hutchinson
No abstract text is available yet for this article.
October 11, 2016: Nature Reviews. Clinical Oncology
https://www.readbyqxmd.com/read/27716525/activation-induced-cytidine-deaminase-mutant-aid-his130pro-from-hyper-igm-2-patient-retained-mutagenic-activity-on-shm-artificial-substrate
#10
Hanen Ouadani, Imen Ben-Mustapha, Meriem Ben-Ali, Beya Larguèche, Tihana Jovanic, Sylvie Garcia, Benoit Arcangioli, Houda Elloumi-Zghal, Dahmani Fathallah, Mongia Hachicha, Hatem Masmoudi, François Rougeon, Mohamed-Ridha Barbouche
Activation induced cytidine deaminase (AID) is an essential enzyme for class switch recombination (CSR) and somatic hypermutation (SHM) during secondary immune response. Mutations in the AICDA gene are responsible for Hyper IgM 2 syndrome where both CSR and SHM or only CSR are affected. Indeed, triggering either of the two mechanisms requires the DNA deamination activity of AID. Besides, different domains of AID may be differentially involved in CSR and SHM through their interaction with specific cofactors...
October 4, 2016: Molecular Immunology
https://www.readbyqxmd.com/read/27716362/dna-replication-stress-a-source-of-apobec3b-expression-in-breast-cancer
#11
David W Cescon, Benjamin Haibe-Kains
APOBEC cytidine deaminases have been implicated as major contributors to the mutation burden in many cancers on the basis of their mutational signature. A new experimental study sheds light on the inciting factors, linking APOBEC3B expression to oncogene- and drug-induced replication stress.
September 30, 2016: Genome Biology
https://www.readbyqxmd.com/read/27694382/apobec3-snps-predict-apobec-mutagenesis-and-cancer-risk
#12
(no author information available yet)
SNPs in APOBEC3 alter expression of APOBEC3A/APOBEC3B to affect somatic APOBEC-signature mutations.
September 30, 2016: Cancer Discovery
https://www.readbyqxmd.com/read/27650891/the-dna-cytosine-deaminase-apobec3h-haplotype-i-likely-contributes-to-breast-and-lung-cancer-mutagenesis
#13
Gabriel J Starrett, Elizabeth M Luengas, Jennifer L McCann, Diako Ebrahimi, Nuri A Temiz, Robin P Love, Yuqing Feng, Madison B Adolph, Linda Chelico, Emily K Law, Michael A Carpenter, Reuben S Harris
Cytosine mutations within TCA/T motifs are common in cancer. A likely cause is the DNA cytosine deaminase APOBEC3B (A3B). However, A3B-null breast tumours still have this mutational bias. Here we show that APOBEC3H haplotype I (A3H-I) provides a likely solution to this paradox. A3B-null tumours with this mutational bias have at least one copy of A3H-I despite little genetic linkage between these genes. Although deemed inactive previously, A3H-I has robust activity in biochemical and cellular assays, similar to A3H-II after compensation for lower protein expression levels...
September 21, 2016: Nature Communications
https://www.readbyqxmd.com/read/27647909/whole-exome-sequencing-identifies-multiple-loss-of-function-mutations-of-nf-%C3%AE%C2%BAb-pathway-regulators-in-nasopharyngeal-carcinoma
#14
Hong Zheng, Wei Dai, Arthur Kwok Leung Cheung, Josephine Mun Yee Ko, Rebecca Kan, Bonnie Wing Yan Wong, Merrin Man Long Leong, Mingdan Deng, Tommy Chin Tung Kwok, Jimmy Yu-Wai Chan, Dora Lai-Wan Kwong, Anne Wing-Mui Lee, Wai Tong Ng, Roger Kai Cheong Ngan, Chun Chung Yau, Stewart Tung, Victor Ho-Fun Lee, Ka-On Lam, Chung Kong Kwan, Wing Sum Li, Stephen Yau, Kwok-Wah Chan, Maria Li Lung
Nasopharyngeal carcinoma (NPC) is an epithelial malignancy with a unique geographical distribution. The genomic abnormalities leading to NPC pathogenesis remain unclear. In total, 135 NPC tumors were examined to characterize the mutational landscape using whole-exome sequencing and targeted resequencing. An APOBEC cytidine deaminase mutagenesis signature was revealed in the somatic mutations. Noticeably, multiple loss-of-function mutations were identified in several NF-κB signaling negative regulators NFKBIA, CYLD, and TNFAIP3 Functional studies confirmed that inhibition of NFKBIA had a significant impact on NF-κB activity and NPC cell growth...
October 4, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27643540/association-of-germline-variants-in-the-apobec3-region-with-cancer-risk-and-enrichment-with-apobec-signature-mutations-in-tumors
#15
Candace D Middlebrooks, A Rouf Banday, Konichi Matsuda, Krizia-Ivana Udquim, Olusegun O Onabajo, Ashley Paquin, Jonine D Figueroa, Bin Zhu, Stella Koutros, Michiaki Kubo, Taro Shuin, Neal D Freedman, Manolis Kogevinas, Nuria Malats, Stephen J Chanock, Montserrat Garcia-Closas, Debra T Silverman, Nathaniel Rothman, Ludmila Prokunina-Olsson
High rates of APOBEC-signature mutations are found in many tumors, but factors affecting this mutation pattern are not well understood. Here we explored the contribution of two common germline variants in the APOBEC3 region. SNP rs1014971 was associated with bladder cancer risk, increased APOBEC3B expression, and enrichment with APOBEC-signature mutations in bladder tumors. In contrast, a 30-kb deletion that eliminates APOBEC3B and creates an APOBEC3A-APOBEC3B chimera was not important in bladder cancer, whereas it was associated with breast cancer risk and enrichment with APOBEC-signature mutations in breast tumors...
September 19, 2016: Nature Genetics
https://www.readbyqxmd.com/read/27603796/activating-the-innate-immune-response-to-counter-chronic-hepatitis-b-virus-infection
#16
Camilla Lamb, Patrick Arbuthnot
INTRODUCTION: Chronic infection with hepatitis B virus (HBV) is endemic to several populous parts of the world, where resulting complicating cirrhosis and hepatocellular carcinoma occur commonly. Licensed drugs to treat the infection have limited curative efficacy, and development of therapies that eliminate all replication intermediates of HBV is a priority. AREAS COVERED: The recent demonstration that the activation of the innate immune response may eradicate HBV from infected hepatocytes has a promising therapeutic application...
September 7, 2016: Expert Opinion on Biological Therapy
https://www.readbyqxmd.com/read/27585283/functions-and-malfunctions-of-mammalian-dna-cytosine-deaminases
#17
Sachini U Siriwardena, Kang Chen, Ashok S Bhagwat
The AID/APOBEC family enzymes convert cytosines in single-stranded DNA to uracils, causing base substitutions and strand breaks. They are induced by cytokines produced during the body's inflammatory response to infections, and they help combat infections through diverse mechanisms. AID is essential for the maturation of antibodies and causes mutations and deletions in antibody genes through somatic hypermutation (SHM) and class-switch recombination (CSR) processes. One member of the APOBEC family, APOBEC1, edits mRNA for a protein involved in lipid transport...
September 1, 2016: Chemical Reviews
https://www.readbyqxmd.com/read/27558125/ifn-stimulated-gene-expression-is-independent-of-the-ifnl4-genotype-in-chronic-hiv-1-infection
#18
Katia Monteleone, Giuseppe Corano Scheri, Maura Statzu, Carla Selvaggi, Francesca Falasca, Noemi Giustini, Ivano Mezzaroma, Ombretta Turriziani, Gabriella d'Ettorre, Guido Antonelli, Carolina Scagnolari
This study aimed to evaluate the association between the IFNL4 rs368234815 (ΔG/TT) dinucleotide polymorphism and the IFN response during chronic HIV-1 infection. We carried out genotyping analysis and measured the expression of IFN-stimulated genes (ISGs) (myxovirus resistance protein A [MxA], ISG15, ISG56, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like [APOBEC] 3F and APOBEC3G) on peripheral blood mononuclear cells collected from naïve and HAART-treated HIV-1-infected patients. There were no statistically significant differences in endogenous ISGs mRNA levels among HIV-1-positive patients bearing different IFNL4 genotypes, suggesting that ISG expression is independent of the IFNL4 genotype in HIV-1 infection...
November 2016: Archives of Virology
https://www.readbyqxmd.com/read/27545006/elucidating-genomic-characteristics-of-lung-cancer-progression-from-in-situ-to-invasive-adenocarcinoma
#19
Chanida Vinayanuwattikun, Florence Le Calvez-Kelm, Behnoush Abedi-Ardekani, David Zaridze, Anush Mukeria, Catherine Voegele, Maxime Vallée, Dewajani Purnomosari, Nathalie Forey, Geoffroy Durand, Graham Byrnes, James Mckay, Paul Brennan, Ghislaine Scelo
To examine the diversity of somatic alterations and clonal evolution according to aggressiveness of disease, nineteen tumor-blood pairs of 'formerly bronchiolo-alveolar carcinoma (BAC)' which had been reclassified into preinvasive lesion (adenocarcinoma in situ; AIS), focal invasive lesion (minimally invasive adenocarcinoma; MIA), and invasive lesion (lepidic predominant adenocarcinoma; LPA and non-lepidic predominant adenocarcinoma; non-LPA) according to IASLC/ATS/ERS 2011 classification were explored by whole exome sequencing...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27527602/aid-apobec-network-reconstruction-identifies-pathways-associated-with-survival-in-ovarian-cancer
#20
Martin Svoboda, Anastasia Meshcheryakova, Georg Heinze, Markus Jaritz, Dietmar Pils, Dan Cacsire Castillo-Tong, Gudrun Hager, Theresia Thalhammer, Erika Jensen-Jarolim, Peter Birner, Ioana Braicu, Jalid Sehouli, Sandrina Lambrechts, Ignace Vergote, Sven Mahner, Philip Zimmermann, Robert Zeillinger, Diana Mechtcheriakova
BACKGROUND: Building up of pathway-/disease-relevant signatures provides a persuasive tool for understanding the functional relevance of gene alterations and gene network associations in multifactorial human diseases. Ovarian cancer is a highly complex heterogeneous malignancy in respect of tumor anatomy, tumor microenvironment including pro-/antitumor immunity and inflammation; still, it is generally treated as single disease. Thus, further approaches to investigate novel aspects of ovarian cancer pathogenesis aiming to provide a personalized strategy to clinical decision making are of high priority...
2016: BMC Genomics
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