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Academic literature on the topic 'Deaminases'

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Published: 10 March 2023
Last updated: 14 March 2023

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Journal articles on the topic "Deaminases"

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Rogozin, Igor, Abiel Roche-Lima, Artem Lada, Frida Belinky, Ivan Sidorenko, Galina Glazko, Vladimir Babenko, David Cooper, and Youri Pavlov. "Nucleotide Weight Matrices Reveal Ubiquitous Mutational Footprints of AID/APOBEC Deaminases in Human Cancer Genomes." Cancers 11, no. 2 (February 12, 2019): 211. http://dx.doi.org/10.3390/cancers11020211.

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Cancer genomes accumulate nucleotide sequence variations that number in the tens of thousands per genome. A prominent fraction of these mutations is thought to arise as a consequence of the off-target activity of DNA/RNA editing cytosine deaminases. These enzymes, collectively called activation induced deaminase (AID)/APOBECs, deaminate cytosines located within defined DNA sequence contexts. The resulting changes of the original C:G pair in these contexts (mutational signatures) provide indirect evidence for the participation of specific cytosine deaminases in a given cancer type. The conventional method used for the analysis of mutable motifs is the consensus approach. Here, for the first time, we have adopted the frequently used weight matrix (sequence profile) approach for the analysis of mutagenesis and provide evidence for this method being a more precise descriptor of mutations than the sequence consensus approach. We confirm that while mutational footprints of APOBEC1, APOBEC3A, APOBEC3B, and APOBEC3G are prominent in many cancers, mutable motifs characteristic of the action of the humoral immune response somatic hypermutation enzyme, AID, are the most widespread feature of somatic mutation spectra attributable to deaminases in cancer genomes. Overall, the weight matrix approach reveals that somatic mutations are significantly associated with at least one AID/APOBEC mutable motif in all studied cancers.
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Seffernick, Jennifer L., Anthony G. Dodge, Michael J. Sadowsky, John A. Bumpus, and Lawrence P. Wackett. "Bacterial Ammeline Metabolism via Guanine Deaminase." Journal of Bacteriology 192, no. 4 (December 18, 2009): 1106–12. http://dx.doi.org/10.1128/jb.01243-09.

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ABSTRACT Melamine toxicity in mammals has been attributed to the blockage of kidney tubules by insoluble complexes of melamine with cyanuric acid or uric acid. Bacteria metabolize melamine via three consecutive deamination reactions to generate cyanuric acid. The second deamination reaction, in which ammeline is the substrate, is common to many bacteria, but the genes and enzymes responsible have not been previously identified. Here, we combined bioinformatics and experimental data to identify guanine deaminase as the enzyme responsible for this biotransformation. The ammeline degradation phenotype was demonstrated in wild-type Escherichia coli and Pseudomonas strains, including E. coli K12 and Pseudomonas putida KT2440. Bioinformatics analysis of these and other genomes led to the hypothesis that the ammeline deaminating enzyme was guanine deaminase. An E. coli guanine deaminase deletion mutant was deficient in ammeline deaminase activity, supporting the role of guanine deaminase in this reaction. Two guanine deaminases from disparate sources (Bradyrhizobium japonicum USDA 110 and Homo sapiens) that had available X-ray structures were purified to homogeneity and shown to catalyze ammeline deamination at rates sufficient to support bacterial growth on ammeline as a sole nitrogen source. In silico models of guanine deaminase active sites showed that ammeline could bind to guanine deaminase in a similar orientation to guanine, with a favorable docking score. Other members of the amidohydrolase superfamily that are not guanine deaminases were assayed in vitro, and none had substantial ammeline deaminase activity. The present study indicated that widespread guanine deaminases have a promiscuous activity allowing them to catalyze a key reaction in the bacterial transformation of melamine to cyanuric acid and potentially contribute to the toxicity of melamine.
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Vasudevan, Ananda Ayyappan Jaguva, Sander H. J. Smits, Astrid Höppner, Dieter Häussinger, Bernd W. Koenig, and Carsten Münk. "Structural features of antiviral DNA cytidine deaminases." Biological Chemistry 394, no. 11 (November 1, 2013): 1357–70. http://dx.doi.org/10.1515/hsz-2013-0165.

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Abstract The APOBEC3 (A3) family of cytidine deaminases plays a vital role for innate defense against retroviruses. Lentiviruses such as HIV-1 evolved the Vif protein that triggers A3 protein degradation. There are seven A3 proteins, A3A-A3H, found in humans. All A3 proteins can deaminate cytidines to uridines in single-stranded DNA (ssDNA), generated during viral reverse transcription. A3 proteins have either one or two cytidine deaminase domains (CD). The CDs coordinate a zinc ion, and their amino acid specificity classifies the A3s into A3Z1, A3Z2, and A3Z3. A3 proteins occur as monomers, dimers, and large oligomeric complexes. Studies on the nature of A3 oligomerization, as well as the mode of interaction of A3s with RNA and ssDNA are partially controversial. High-resolution structures of the catalytic CD2 of A3G and A3F as well as of the single CD proteins A3A and A3C have been published recently. The NMR and X-ray crystal structures show globular proteins with six α-helices and five β sheets arranged in a characteristic motif (α1-β1-β2/2′-α2-β3-α3-β4-α4-β5-α5-α6). However, the detailed arrangement and extension of individual structure elements and their relevance for A3 complex formation and activity remains a matter of debate and will be highlighted in this review.
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Teperek-Tkacz, Marta, Vincent Pasque, George Gentsch, and Anne C. Ferguson-Smith. "Epigenetic reprogramming: is deamination key to active DNA demethylation?" REPRODUCTION 142, no. 5 (November 2011): 621–32. http://dx.doi.org/10.1530/rep-11-0148.

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DNA demethylation processes are important for reproduction, being central in epigenetic reprogramming during embryonic and germ cell development. While the enzymes methylating DNA have been known for many years, identification of factors capable of mediating active DNA demethylation has been challenging. Recent findings suggest that cytidine deaminases may be key players in active DNA demethylation. One of the most investigated candidates is activation-induced cytidine deaminase (AID), best known for its role in generating secondary antibody diversity in B cells. We evaluate evidence for cytidine deaminases in DNA demethylation pathways in vertebrates and discuss possible models for their targeting and activity regulation. These findings are also considered along with alternative demethylation pathways involving hydroxymethylation.
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Roth, E. Jr, N. Ogasawara, and S. Schulman. "The deamination of adenosine and adenosine monophosphate in Plasmodium falciparum-infected human erythrocytes: in vitro use of 2'deoxycoformycin and AMP deaminase-deficient red cells." Blood 74, no. 3 (August 15, 1989): 1121–25. http://dx.doi.org/10.1182/blood.v74.3.1121.1121.

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Abstract The role of enzymatic deamination of adenosine monophosphate (AMP) and adenosine in the in vitro growth of the malaria parasite Plasmodium falciparum was investigated by means of human red cells deficient in AMP deaminase to which the adenosine deaminase inhibitor 2′- deoxycoformycin was added. Malaria parasites grew normally in red cells lacking one or both of these enzyme activities. As a further probe of adenosine triphosphate (ATP) catabolism, both infected and uninfected RBCs were incubated with NaF (with and without 2′-deoxycoformycin) and the purine nucleotide/nucleoside content was analyzed by high- performance liquid chromatography (HPLC). Uninfected RBCs lacking either AMP or adenosine deaminase were able to bypass the enzyme block and degrade ATP to hypoxanthine. Uninfected RBCs with both deaminases blocked were unable to produce significant quantities of hypoxanthine. On the other hand, infected RBCs were able to bypass blockade of both deaminases and produce hypoxanthine and adenosine. These findings establish that deamination of adenosine and/or AMP are not essential for plasmodial growth. However, further work will be required to elucidate the pathways that permit the parasites to bypass these catabolic steps.
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Roth, E. Jr, N. Ogasawara, and S. Schulman. "The deamination of adenosine and adenosine monophosphate in Plasmodium falciparum-infected human erythrocytes: in vitro use of 2'deoxycoformycin and AMP deaminase-deficient red cells." Blood 74, no. 3 (August 15, 1989): 1121–25. http://dx.doi.org/10.1182/blood.v74.3.1121.bloodjournal7431121.

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The role of enzymatic deamination of adenosine monophosphate (AMP) and adenosine in the in vitro growth of the malaria parasite Plasmodium falciparum was investigated by means of human red cells deficient in AMP deaminase to which the adenosine deaminase inhibitor 2′- deoxycoformycin was added. Malaria parasites grew normally in red cells lacking one or both of these enzyme activities. As a further probe of adenosine triphosphate (ATP) catabolism, both infected and uninfected RBCs were incubated with NaF (with and without 2′-deoxycoformycin) and the purine nucleotide/nucleoside content was analyzed by high- performance liquid chromatography (HPLC). Uninfected RBCs lacking either AMP or adenosine deaminase were able to bypass the enzyme block and degrade ATP to hypoxanthine. Uninfected RBCs with both deaminases blocked were unable to produce significant quantities of hypoxanthine. On the other hand, infected RBCs were able to bypass blockade of both deaminases and produce hypoxanthine and adenosine. These findings establish that deamination of adenosine and/or AMP are not essential for plasmodial growth. However, further work will be required to elucidate the pathways that permit the parasites to bypass these catabolic steps.
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Jost, Stéphanie, Priscilla Turelli, Bastien Mangeat, Ulrike Protzer, and Didier Trono. "Induction of Antiviral Cytidine Deaminases Does Not Explain the Inhibition of Hepatitis B Virus Replication by Interferons." Journal of Virology 81, no. 19 (July 25, 2007): 10588–96. http://dx.doi.org/10.1128/jvi.02489-06.

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ABSTRACT Interferons (IFNs) play a major role in the control of hepatitis B virus (HBV), whether as endogenous cytokines limiting the spread of the virus during the acute phase of the infection or as drugs for the treatment of its chronic phase. However, the mechanism by which IFNs inhibit HBV replication has so far remained elusive. Here, we show that type I and II IFN treatment of human hepatocytes induces the production of APOBEC3G (A3G) and, to a lesser extent, that of APOBEC3F (A3F) and APOBEC3B (A3B) but not that of two other cytidine deaminases also endowed with anti-HBV activity, activation-induced cytidine deaminase (AID), and APOBEC1. Most importantly, we reveal that blocking A3B, A3F, and A3G by combining RNA interference and the virion infectivity factor (Vif) protein of human immunodeficiency virus does not abrogate the inhibitory effect of IFNs on HBV. We conclude that these cytidine deaminases are not essential effectors of IFN in its action against this pathogen.
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Liu, Lei, Jian-Feng Wu, Ying-Fei Ma, Sheng-Yue Wang, Guo-Ping Zhao, and Shuang-Jiang Liu. "A Novel Deaminase Involved in Chloronitrobenzene and Nitrobenzene Degradation with Comamonas sp. Strain CNB-1." Journal of Bacteriology 189, no. 7 (January 26, 2007): 2677–82. http://dx.doi.org/10.1128/jb.01762-06.

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ABSTRACT Comamonas sp. strain CNB-1 degrades nitrobenzene and chloronitrobenzene via the intermediates 2-aminomuconate and 2-amino-5-chloromuconate, respectively. Deamination of these two compounds results in the release of ammonia, which is used as a source of nitrogen for bacterial growth. In this study, a novel deaminase was purified from Comamonas strain CNB-1, and the gene (cnbZ) encoding this enzyme was cloned. The N-terminal sequence and peptide fingerprints of this deaminase were determined, and BLAST searches revealed no match with significant similarity to any functionally characterized proteins. The purified deaminase is a monomer (30 kDa), and its V max values for 2-aminomuconate and 2-amino-5-chloromuconate were 147 μmol·min−1·mg−1 and 196 μmol·min−1·mg−1, respectively. Its catalytic products from 2-aminomuconate and 2-amino-5-chloromuconate were 2-hydroxymuconate and 2-hydroxy-5-chloromuconate, respectively, which are different from those previously reported for the deaminases of Pseudomonas species. In the catalytic mechanism proposed, the α-carbon and nitrogen atoms (of both 2-aminomuconate and 2-amino-5-chloromuconate) were simultaneously attacked by a hydroxyl group and a proton, respectively. Homologs of cnbZ were identified in the genomes of Bradyrhizobium japonicum, Rhodopseudomonas palustris, and Roseiflexus sp. strain RS-1; these genes were previously annotated as encoding hypothetical proteins of unknown function. It is concluded that CnbZ represents a novel enzyme that deaminates xenobiotic compounds and/or α-amino acids.
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Mahieux, Renaud, Rodolphe Suspène, Frédéric Delebecque, Michel Henry, Olivier Schwartz, Simon Wain-Hobson, and Jean-Pierre Vartanian. "Extensive editing of a small fraction of human T-cell leukemia virus type 1 genomes by four APOBEC3 cytidine deaminases." Journal of General Virology 86, no. 9 (September 1, 2005): 2489–94. http://dx.doi.org/10.1099/vir.0.80973-0.

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In the absence of the human immunodeficiency virus type 1 (HIV-1) Vif protein, the host-cell cytidine deaminases APOBEC3F and -3G are co-packaged along with virion RNA. Upon infection of target cells, nascent single-stranded DNA can be edited extensively, invariably giving rise to defective genomes called G→A hypermutants. Although human T-cell leukemia virus type 1 (HTLV-1) replicates in the same cell type as HIV-1, it was shown here that HTLV-1 is relatively resistant to the antiviral effects mediated by human APOBEC3B, -3C, -3F and -3G. Nonetheless, a small percentage of genomes (0·1<f<5 %) were edited extensively: up to 97 % of cytidine targets were deaminated. In contrast, hypermutated HTLV-1 genomes were not identified in peripheral blood mononuclear cell DNA from ten patients with non-malignant HTLV-1 infection. Thus, although HTLV-1 DNA can indeed be edited by at least four APOBEC3 cytidine deaminases in vitro, they are conspicuously absent in vivo.
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Morgan, Hugh D., Wendy Dean, Heather A. Coker, Wolf Reik, and Svend K. Petersen-Mahrt. "Activation-induced Cytidine Deaminase Deaminates 5-Methylcytosine in DNA and Is Expressed in Pluripotent Tissues." Journal of Biological Chemistry 279, no. 50 (September 24, 2004): 52353–60. http://dx.doi.org/10.1074/jbc.m407695200.

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DNA deaminases of the Aid/Apobec family convert cytosine into uracil and play key roles in acquired and innate immunity. The epigenetic modification by methylation of cytosine in CpG dinucleotides is also mutagenic, but this is thought to occur by spontaneous deamination. Here we show that Aid and Apobec1 are 5-methylcytosine deaminases resulting in a thymine base opposite a guanine. Their action can thus lead to C → T transition mutations in methylated DNA, or in conjunction with repair of the T:G mismatch, to demethylation. TheAidandApobec1genes are located in a cluster of pluripotency genes includingNanogandStellaand are co-expressed with these genes in oocytes, embryonic germ cells, and embryonic stem cells. These results suggest that Aid and perhaps some of its family members may have roles in epigenetic reprogramming and cell plasticity. Transition in CpG dinucleotides is the most frequent mutation in human genetic diseases, and sequence context analysis of CpG transitions in the APC tumor suppressor gene suggests that DNA deaminases may play a significant role in tumor etiology.
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Dissertations / Theses on the topic "Deaminases"

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Wang, Meng. "Mutational analysis of DNA deaminases." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611829.

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Beale, R. C. L. "DNA sequence specificity of APOBEC family deaminases." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596493.

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APOBEC family deaminases are capable of causing mutations by deaminating cytosine in DNA to uracil. This is exploited in diversification of the repertoire of antibodies by somatic hypermutation, and also in restricting the spread of retroviruses. APOBEC family induced mutations are not distributed entirely at random throughout the genes they deaminate; rather each APOBEC family member has its own preferred local sequence that will be preferentially targeted. Work presented in this thesis elucidates these preferred motifs for a number of different deaminases and investigates the structural basis of their specificity using viral and bacterial genetic assays. To determine the local sequence specificities of APOBEC proteins active in E. coli, a novel selection system was devised based on the conditional-lethal sacB gene. By varying the activity and orientation of promoters it was possible to target mutations to a chromosomally integrated sacB gene under certain conditions. Selecting for viable mutants generated mutation spectra for the AID, APOBEC1 and APOBEC3G deaminases. This enabled their preferred sequence motifs to be identified and correlated with particular mutation patterns found in vivo.
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Lembo, Gaia. "Substrate targeting and inhibition of editing deaminases." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1144295.

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Identification of small molecules against APOBEC3B The APOBECs are deaminases that act on DNA and RNA to restrict exogenous nucleic acids. Yet, the signature of their mutagenic activity –especially that of APOBEC3A and APOBEC3B- has been observed in the cancer genomes and their ability to increase the genetic heterogeneity of tumours has been linked to the onset of drug resistance in cancer. As such inhibition of their enzymatic activity represents a potential target for anticancer therapies. During my PhD I worked at the identification of APOBEC3B small-molecule inhibitors. To this aim, I used a computational approach to perform a virtual screening on large library of molecules to block APOBEC3B enzymatic activity. I then tested selected molecules from the virtual screening using biochemical assays to quantify their effect on APOBEC3B activity and their capacity to interfere with APOBEC3B binding to DNA. Through this, I was able to identify two small molecules that reduce the activity of this protein, which could provide basis for the development of the first drug for anti-APOBEC activity. Engineering ADAR2 to act on DNA Genome editing technologies have revolutionized our ability to target and modify the genomes of living cells and organisms. The fusion of AID/APOBECs to genome editing tools such as Cas9 allowed the development the first base editor, molecules that can be targeted to mutate specific cytosines. The pool of available Base Editors is in constant expansion as new molecules are developed to target DNA with more specificity and efficiency. As the only adenine-targeting Base Editor is based on TadA- an RNA deaminase-, I focused on the development of a A•T base editor based on the catalytic domain of ADAR2. Adenosine Deaminases Acting on RNA (ADARs), are editing enzymes that catalyse the C6 deamination of adenosine (A) to produce inosine (I) in double-stranded RNA. As human ADAR2 is able to target DNA/RNA hybrids, I first tried -without success- to use chimeras of n/dCas9 and the deaminase domain of ADAR2 to induce mutations in a fluorescent reporter. I then used a bacterial screen to select for mutants of ADAR2 that act on DNA. I selected a mutant that induces a mutator phenotype in bacteria and DNA damage in mammalian cells. I am currently working to engineer this mutant into a Base Editor suitable for biotechnological applications such as gene therapy, antiviral treatment and cancer therapy.
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Hogg, Marion. "Characterising new roles for APOBEC4 and ADAR deaminases." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4792.

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Deamination or the hydrolytic removal of one hydroxyl group from a base in DNA or RNA can lead to changes in the transcript and protein produced. Examples of this are the deamination of cytosine residues in DNA by activation induced deaminase (AID) during antibody diversification, or deamination of adenosine at the Q/R site in the GluR-B transcript by adenosine deaminase acting on RNA 2 (ADAR2), which regulates calcium permeability in neurons. The initial focus of my thesis was to characterise a putative novel deaminase APOBEC4. APOBEC4 was identified in a bioinformatic search for proteins containing the core catalytic residues common to the whole family of Cytidine Deaminase enzymes. The aim of the project was to express and purify recombinant APOBEC4 for in vitro characterization, however despite using different expression systems and purification conditions the majority of the recombinant protein was inherently insoluble and I could not isolate sufficient amounts of protein for further studies. Recombinant protein with a GST-tag was used to generate polyclonal antibodies which recognised recombinant protein but were unable to detect endogenous APOBEC4. The focus of my thesis then changed to the process of adenosine to inosine editing in RNA, which is a post-transcriptional mechanism for generating protein diversity. The enzyme family responsible for catalysing this reaction is known as ADAR, and Drosophila melanogaster has only one Adar gene. Flies lacking the Adar gene show locomotion defects and age-dependent neurodegeneration, however little is known about the molecular mechanism underlying these defects. To investigate this phenotype I performed microarray analysis on RNA isolated from heads of 5 day old flies lacking the Adar gene to characterize gene expression changes in the fly heads before neurodegeneration caused secondary effects. Analysis was also performed on Adar-null flies expressing either an active Adar gene or a catalytically-inactive Adar gene in cholinergic neurons to determine which transcripts could be directly regulated by Adar. I confirmed the microarray results by real-time PCR, and demonstrated that the changes in transcript level could be reversed by expression of either active or catalytically-inactive Adar. Expression of edited transcripts did not change dramatically. Filter-binding analysis and electrophoretic mobility shift assay revealed that recombinant ADAR could bind to all RNA transcripts analysed with similar affinity; both known substrates and potential new substrates for Adar, as well as transcripts that were chosen as negative controls due to their expression not altering in the expression microarray. Recombinant ADAR bound to dsRNA with a very high affinity; other transcripts investigated bound with considerably lower affinity, yet all transcripts investigated were bound by ADAR. Further analysis of transcript changes in Adar-null flies was investigated by performing microarray analysis with a custom-made splicing-sensitive microarray. Analysis revealed that a subset of transcripts were differentially spliced in Adar-null flies; however this group of transcripts was distinct from the group identified as being altered on the expression microarray, indicating that the splicing changes are independent of changes in expression. Analysis of exon-specific probes on the splicing array confirmed the transcript changes identified in the expression array. Real-time PCR confirmed the changes in splicing, and these transcripts were further examined by sequence analysis. This revealed several transcripts identified as altered by the AS array showed use of alternative polyadenylation sites indicating ADAR may have a role in detemining polyadenylation site selection.
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Torrini, Serena. "Physiological and pathological perspectives in the biology of APOBEC deaminases." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1194433.

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The thesis is focus on RNA editing mediated by two AID/APOBEC family members. The aim of my work was the investigation of possible novel factors that regulate hAPOBEC1 expression or cofactors which help the deaminase to exert its activity. First, I characterised cellular models for their proliferation and clonogenic activities as well as cell cycle distribution evaluating a combinatorial effect of hAPOBEC1 and RBM47 which lead to a decrease in cell growth. I investigated the role of RNA editing beyond the lipid transport by high-throughput sequencing which provided me information regarding new deamination events, RNA stability, and also a differential gene expression in presence or absence of the editosome components. By Differential expression analysis, I got a list of genes that are differentially expressed in clones with hAPOBEC1 and RBM47 which need to be analysed for their biological meaning. From the mRNA-seq I got a consistent list of putative edited sites even though some of them were validated with no success. Moreover, I applied a genetic library screen to activate a high number of genes in cells expressing RBM47 to evaluate an eventual up-regulation of APOBEC1 and find factors which trigger its expression. The cells in which editing happened have been selected thanks to a specific fluorescent reporter containing ApoB target. The results have still to be analysed. The second aim of my project was to study APOBEC3A regulation, by chemical and genetic screenings, through the development of a specific sensitive reporter system to detect APOBEC3A-mediated RNA editing. In this work I presented the design of an artificial fluorescent reporter containing a target of APOBEC3A like SDHB or DDOST properly built to produce a stop codon in the middle of the target and optimised for the levels of editing. I checked its specificity for APOBEC3A and not for other APOBEC proteins like APOBEC1 and APOBEC3B. This let me also detected a novel putative editing site mediated by APOBEC3A by Sanger sequencing. Moreover, I designed another fluorescent reporter system able to evaluate APOBEC3A RNA editing by fluorescent microscopy. I created stable cell lines expressing all the lentiviral reporter plasmids to further investigate induction of endogenous APOBEC3A and its regulation. In a future perspective the dual fluorescent reporter could be a useful tool to identify novel RNA editing targets upon the application of an activation library screen.
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Giorgio, Salvatore Di. "Computational approaches for the identification of APOBEC1- dependent RNA editing events in human tissues." Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1096840.

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The AID/APOBECs are cytosine deaminases involved in diverse physiological contexts through their ability to edit DNA and RNA. This ability comes with a price: Activation-Induce cytidine Deaminase (AID), the main player in the antibody diversification processes, is responsible for some of the common genetic alterations in mature B-cells tumours; the APOBEC3 subgroup, important actors in virus defence, have been linked to different mutational processes in a number of cancers. Also APOBEC1, an RNA/DNA editing enzyme, also able to restrict lentivirus and mobile elements, can act as a mutator in human cells, and its aberrant expression could be linked to the onset of alterations both at the genomic and transcriptomic level. APOBEC1 RNA editing is a post transcriptional process, its only well-characterized target is the Apolipoprotein B transcript (ApoB) in the small intestine where editing of C6666 induces formation of a stop codon and translation of a truncated protein. Quite different is the situation in Rodents where, thanks to the availability of APOBEC1 knockout mice, hundreds of APOBEC1-dependent editing events, have been discovered beyond ApoB. To date, APOBEC1 deficiencies are not known and in humans and only a few transcripts have been added to the list of targets. Despite the targets known in mice and in humans, we are far from understanding the overall physiological meaning of APOBEC1-induced C to U editing. If we exclude the efforts that have been made to identify and characterise C to U editing in rodents, only few computational approaches have been employed to identify and characterize human APOBEC1 targets. This is the reason why I have used available human RNA-seq data to develop a computational strategy for the identification of APOBEC1 dependent RNA editing events. I used The Cancer Genome Atlas (TCGA) and The Genotype-Tissue Expression (GTEX) to obtain datasets of samples in which APOBEC1 is expressed at different levels. Using these datasets, I divided samples in high and low expression levels of APOBEC1, and through known tools and ad hoc scripts I built different pipelines to identify positions in the transcript that are differentially edited. The pipeline includes several filters: removal of mapping artefacts, germline and somatic single nucleotide variants, removal of homopolymeric regions and so on. Among the several strategies I used, the most promising are those applied to the GTEX small intestine data, where a strict analysis has shown the presence of at least 12 sites, including 3 known targets on the ApoB mRNA. Surprisingly we found evidence of ApoB editing at canonical sites beyond the small intestine, even in absence of measurable APOBEC1 expression. Considering the possible presence of APOBEC1 outside the gastric tissue, to improve our capacity to identify C to U editing in human tissues, I decided to create a database of C>U edited sites using RNA-seq from APOBEC1 -transfected Hek293T cell lines. This database, despite not representing physiologically edited sites, it informs on all positions biologically editable. Crossing these positions with those obtained from the GTEX dataset results in the identification of hundreds of common edited sites. Finally, I tested the hypothesis that APOBEC1 editing affects the transcript stability in Hek293T cells. Preliminary data suggest that APOBEC1 expression could shift the equilibrium between processed RNA and non-processed RNA towards the latter one. The second part of the thesis centers on the study of RNA-off targets induced by Base editors (BEs). In order to improve the safety of this powerful genome editing tool, another PhD student in the lab, Francesco Donati, selected several APOBEC1 mutant that are not able to edit the RNA while maintaining their mutagenicity on DNA. He investigated both the tumorigenicity of these mutants in mice and their use in genome editing. He obtained exonic and transcriptomic data from murine liver tumors and from cells overexpressing the mutant base editors, respectively. I performed the bioinformatic analyses to explore the mutational signature induced by APOBEC1 in mice, and to assess the off-targets effects on RNA and DNA of these base editors. I demonstrated that -contrarily to wild-type APOBEC1- these mutants provide the ability to perform genome editing in absence of detectable off-targets.
The 2019-nCoV outbreak has become a global health risk. Editing by host deaminases is an innate restriction process to counter viruses, and it is not yet known whether it operates against coronaviruses. Here we analyze RNA sequences from bronchoalveolar lavage fluids derived from two Wuhan patients. We identify nucleotide changes that may be signatures of RNA editing: Adenosine-to-Inosine changes from ADAR deaminases and Cytosine-to-Uracil changes from APOBEC ones. A mutational analysis of genomes from different strains of human-hosted Coronaviridae reveals patterns similar to the RNA editing pattern observed in the 2019-nCoV transcriptomes. Our results suggest that both APOBECs and ADARs are involved in Coronavirus genome editing, a process that may shape the fate of both virus and patient.
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Periyasamy, Manikandan. "Cytidine deaminases are regulators of estrogen receptor activity in breast cancer cells." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9217.

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Breast cancer is the most common cancer worldwide, with 1.38 million women diagnosed with the disease each year. Estrogens play a critical role in the development and progression of breast cancer, their action being mediated by the estrogen receptors (ER), ERα and ERß, which are the members of the nuclear receptor superfamily of transcription factors. This understanding has led to the development of endocrine therapies aimed at inhibiting ER action by competitive binding to the ER (anti-estrogens), or using inhibitors of estrogen biosynthesis (aromatase inhibitors). Determining the mechanisms by which ER regulate gene expression will aid our understanding of the role of ER in breast cancer progression, response and resistance to endocrine therapies. Upon binding estrogen, ER drives the expression of estrogen responsive genes through the orderly recruitment of co-regulators that act by remodelling and modifying chromatin, ultimately promoting RNA polymerase II recruitment and transcription initiation. Previous work from our laboratory has shown that the APOBEC3B cytosine deaminase acts as an ERα transcriptional coactivator in reporter gene assays. Here, I have developed these initial observations and demonstrate that APOBEC3B is important for the regulation of estrogen responsive genes and breast cancer cell growth. I show that APOBEC3B is recruited to the promoters of estrogen-responsive genes and interacts with ERα. Studies carried out to identify the molecular mechanisms by which APOBEC3B regulates the expression of estrogen-responsive genes included its potential role in DNA demethylation and identified a role for APOBEC3B in DNA strand break formation at the promoter of the estrogen regulated pS2 gene. Together, these studies identify APOBEC3B as an important new coregulator of ERα that is required for the regulation of gene expression by estrogen in breast cancer cells.
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Katsuragi, Tohoru. "Microbial cytosine deaminases and their use in a new kind of cancer chemotherapy." Kyoto University, 1990. http://hdl.handle.net/2433/78236.

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Li, Xianghua. "Physiological roles of Drosophila ADAR and modifiers." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/12225.

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ADAR (Adenosine Deaminases acting on RNA) family proteins are double-strand RNA binding proteins that deaminate specific adenosines into inosines. This A-to-I conversion is called A-to-I RNA editing and is well conserved in the animal kingdom from nematodes to humans. RNA editing is a pre-splicing event on nascent RNA that may affect alternative splicing when the editing occurs in the exon-intron junction or in the intron. Also, editing may change biological function of small RNAs by editing the premicroRNAs or other noncoding RNAs. Editing also alters protein amino acid sequences because inosine in the mRNA base pairs with cytosine and is therefore read as guanosine. In mammals, there are three ADAR family proteins, ADAR1, ADAR2, and ADAR3, encoded by three different genes. So far, no enzymatic activity of ADAR3 is detected. The most frequently edited targets of ADAR1 and ADAR2 are regions covering copies of Alu transposable elements in primates. In addition, loss of some specific editing events leads to profound phenotypes when the editing does not occur correctly. For example, some human neural disorders – such as epilepsy, forebrain ischemia, and Amyotrophic Lateral Sclerosis – are known to be associated with abnormally edited ion channel transcripts. Drosophila has a single ADAR protein (encoded by the Adar gene) that is highly conserved with human ADAR2 (encoded by the ADARB1 gene). To date, 972 editing sites have been identified in 597 transcripts in Drosophila, and approximately 20% of AGO2-associated esiRNAs are edited. Similar to mammals, many ion channel-encoding mRNA transcripts undergo ADAR-mediated A-to-I editing in Drosophila. While Adar1 null mice die at the embryonic stage and Adar2 null mice die shortly after birth due to seizures, Adar null flies are morphologically normal and have normal life span under ideal conditions. However, Adar null flies exhibit severe neurodegeneration and locomotion defects from eclosion, whilst Adar overexpression (OE) is lethal. To better understand the physiological role of RNA editing and ADAR, and to shed light on ADAR-related human disease, I used Drosophila Adar mutant flies as a model organism to investigate phenotypes, and to find chromosomal deletions and specific mutations that rescue the neural-behavioural phenotype of the Adar null mutant flies. Using the publicly available chromosomal deletions collectively covering more than 80% of the euchromatic genome of Chromsome III, I performed a genetic screen to find rescuers of the lethality caused by Adar overexpression. I confirmed that mutation in Rdl (Resistant to dieldrin, the gene encoding GABAA receptor main subunit) rescues. This rescue was not likely caused by effects on Adar expression level or activity. Driven by the hypothesis that the rescue may be due to reduction in GABAergic input to neurons, I recorded spontaneous firing activity of Drosophila larval aCC motor neurons using in vivo extracellular current recording technique. As expected, the neurons overexpressing Adar had much less activities compared with wild type neurons. Also, I found that Adar null fly neurons fired much more and showed epilepsy-like increased excitability. Although feeding PTX (Picrotoxin), a GABAA receptor antagonist, failed to rescue the lethality, reducing the expression of GAD1 to reduce synthesis of GABA was able to rescue the ADAR overexpression lethality. These results suggest that ADAR may finetune neuron activity synergistically with the GABAergic inhibitory signal pathway. I used MARCM (mosaic analysis using a repressible cell marker) to detect cellautonomous phenotypes in Adar null cells in otherwise wild type flies. Although neurodegeneration, observed as enlarged vacuoles formation in neurophils, was detected both in histological staining and EM images, the Adar null neurons marked with GFP from early developmental stages were not lost with age. Nevertheless, swelling in the axons or fragmentation of the axon branches of Adar null neurons was sometimes observed in the midbrain. By comparing the Poly-A RNA sequencing data from Adar null and wild type fly heads, we detected significant upregulation of innate immune genes. I confirmed this by qRT PCR and found that inactive ADAR reduces the innate immune gene transcript levels almost as much as active ADAR does. Further, using the locomotion assay, I confirmed that reintroducing inactive ADAR into Adar null flies can improve the flies’ climbing ability. Based on the Adar null flies having comparatively low viability, I performed a second deficiency screen to find rescuers of Adar null low viability using the same set of deficiencies as in the lethality rescue screen described above. I found seven deletions removing 1 to 37 genes that significantly increased the relative viability of the Adar null flies. However, not all the rescuing deficiencies also improved the Adar null locomotion. One rescuing gene, CG11357 was mapped from one of the rescuing deficiencies, and some mutant alleles of cry, JIL-1 and Gem3 also showed significant effects on the Adar null fly viability. The single gene viability rescuers were also not necessarily locomotion or neurodegeneration rescuers. Although the initial aim was to find neural-behavioural rescuing genes from the viability screen, the viability rescuers found in the screen are more likely to play a role in different aspects of stress response for survival.
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Jaguva, Vasudevan Ananda Ayyappan [Verfasser]. "APOBEC3 DNA deaminases: A mechanistic study of A3A, A3C, and A3G action on retroviruses and counteraction by viral proteins / Ananda Ayyappan Jaguva Vasudevan." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2017. http://d-nb.info/1148720936/34.

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Books on the topic "Deaminases"

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Samuel, Charles E., ed. Adenosine Deaminases Acting on RNA (ADARs) and A-to-I Editing. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-22801-8.

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Palenik, Brian P. Organic nitrogen utilization by phytoplankton: The role of cell-surface deaminases. Woods Hole, Mass: Woods Hole Oceanographic Institution, 1989.

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Adenosine deaminases acting on RNA (ADARs) and A-to-I editing. Heidelberg: Springer, 2012.

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L, Tritsch George, New York Academy of Sciences., and Conference on Adenosine Deaminase in Disorders of Purine Metabolism and in Immune Deficiency (1984 : New York, N.Y.), eds. Adenosine deaminase in disorders of purine metabolism and in immune deficiency. New York, N.Y: New York Academy of Sciences, 1985.

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Chu, Peter Pui Tak. Retroviral-mediated human adenosine deaminase gene transfer into human hematopoietic progenitor and stem cells. Ottawa: National Library of Canada, 1995.

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Thompson, Bridget. Murine acute myeloid leukemia cells expressing the cytosine deaminase gene induce protective immunity to parental leukemic cells. Ottawa: National Library of Canada, 2000.

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Samuel, Charles E. Adenosine Deaminases Acting on RNA and A-to-I Editing. Springer, 2014.

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Samuel, Charles E. Adenosine Deaminases Acting on RNA and A-to-I Editing. Springer, 2011.

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Geha, Raif, and FRED Rosen. Case Studies in Immunology: Adenosine Deaminase Deficiency. W.W. Norton & Company, 2010. http://dx.doi.org/10.4324/9780203853566.

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Geha, Raif, and FRED Rosen. Case Studies in Immunology: Activation-induced Cytidine Deaminase (AID) Deficiency. W.W. Norton & Company, 2010. http://dx.doi.org/10.4324/9780203853535.

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Book chapters on the topic "Deaminases"

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Umbarger, H. E. "Threonine Deaminases." In Advances in Enzymology - and Related Areas of Molecular Biology, 349–95. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/9780470122822.ch6.

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Carter, Charles W. "Nucleoside Deaminases for Cytidine and Adenosine: Comparison with Deaminases Acting on RNA." In Modification and Editing of RNA, 363–75. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818296.ch20.

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Wang, Meng, Cristina Rada, and Michael S. Neuberger. "A High-Throughput Assay for DNA Deaminases." In RNA and DNA Editing, 171–84. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-018-8_11.

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Frazier, Ronald B., and Pang Fai Ma. "A Study of Adenosine Deaminases in Human Sera." In Purine and Pyrimidine Metabolism in Man V, 267–70. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5104-7_43.

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Jantsch, Michael F., and Marie Öhman. "RNA Editing by Adenosine Deaminases that Act on RNA (ADARs)." In Nucleic Acids and Molecular Biology, 51–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-73787-2_3.

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Morse, Daniel P. "Identification of Substrates for Adenosine Deaminases That Act on RNA." In RNA Interference, Editing, and Modification, 199–218. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1385/1-59259-775-0:199.

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Schomburg, Dietmar, and Margit Salzmann. "Cytosine deaminase." In Enzyme Handbook 4, 985–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84437-9_196.

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Schomburg, Dietmar, and Margit Salzmann. "Adenine deaminase." In Enzyme Handbook 4, 989–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84437-9_197.

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Schomburg, Dietmar, and Margit Salzmann. "Guanine deaminase." In Enzyme Handbook 4, 993–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84437-9_198.

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Schomburg, Dietmar, and Margit Salzmann. "Adenosine deaminase." In Enzyme Handbook 4, 999–1003. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84437-9_199.

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Conference papers on the topic "Deaminases"

1

Gordenin, Dmitry A. "Abstract 3577: Pan-cancer analysis of mutagenesis by APOBEC cytidine deaminases." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3577.

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Isquith, Jane, Qingfei Jiang, Raymond Diep, Jessica Pham, Frida Holm, and Catriona Jamieson. "Abstract 3675: Elucidating the role and function of APOBEC3 DNA deaminases in myeloproliferative neoplasms." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3675.

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Isquith, Jane, Qingfei Jiang, Raymond Diep, Jessica Pham, Frida Holm, and Catriona Jamieson. "Abstract 3675: Elucidating the role and function of APOBEC3 DNA deaminases in myeloproliferative neoplasms." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3675.

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Nik-Zainal, Serena, Ben Taylor, Yee Ling Wu, David Wedge, Cristina Rada, Mike Stratton, and Michael Neuberger. "Abstract 611: AID/APOBEC cytidine deaminases can mimic the phenomenon of localized hypermutation in cancer orkataegis." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-611.

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Conner, Kayla L., Asra N. Shaik, Jordan White, Wen Lei, Michele L. Cote, and Steve M. Patrick. "Abstract 3366: APOBEC3 family of cytidine deaminases in sensitizing triple-negative breast cancer cells to cisplatin and carboplatin." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3366.

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Lutfullin, M. T., D. S. Pudova, O. E. Moiseeva, D. L. Zaripova, and A. M. Mardanova. "Genetic determinants responsible for growth-promoting properties of the rhizospheric bacterium Brevibacterium sp. MG-1." In 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.156.

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The paper presents data on sequencing and genome annotations of the Brevibacterium sp. MG-1, capable of synthesizing IAA and siderophores. The genes responsible for the synthesis of ACC deaminase, auxins and hydroxamate type siderophores were identified.
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Pereira, Flávio Ribeiro, Blanca Helena Rios Gomes Bica, Maria Pompeya Olmedo de Lopes de Figueiredo, Rodrigo Lousada, Virginia de Souza Guimarães Merat, Dimona Carvalho Vivas Amado, and Mariana Ferreira Vieira. "Deficiency of Adenosine Deaminase 2: a rare disease." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.2212.

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Sharoyan, S., L. Karapetyan, R. Harutyunyan, S. Mardanyan, and A. Antonyan. "SAT0051 Citrullination of adenosine deaminase isoforms in rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1433.

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Tofovic, Stevan P., Victor Bilan, Edwin K. Jackson, and OLGA Rafikova. "Role Of Plasma Adenosine Deaminase In Hemolysis-Induced Pulmonary Hypertension." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6335.

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PARENTE, JOSÉ SÁVIO MENEZES, AMANDA VIRGINIA BATISTA CAVALCANTE, and THAÍS GUERREIRO JORGE ROCHA. "POLYARTERITIS NODOSA OR DEFICIENCY OF ADENOSINE DEAMINASE 2?: CASE REPORT." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-207.

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Reports on the topic "Deaminases"

1

Steele, Edward J. Deaminases and Why Mice Sometimes Lie in Immuno-Oncology Pre-Clinical Trials? Science Repository, April 2019. http://dx.doi.org/10.31487/j.aco.2019.01.001.

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Mizoguchi, Atsushi. Ectopic Epithelial Deaminase in IBD. Fort Belvoir, VA: Defense Technical Information Center, May 2014. http://dx.doi.org/10.21236/ada610011.

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Mizoguchi, Atsushi. Ectopic Epithelial Deaminase in IBD. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada593311.

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Thomashow, Linda, Leonid Chernin, Ilan Chet, David M. Weller, and Dmitri Mavrodi. Genetically Engineered Microbial Agents for Biocontrol of Plant Fungal Diseases. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7696521.bard.

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The objectives of the project were: a) to construct the site-specific integrative expression cassettes carrying: (i) the chiA gene for a 58-kDa endochitinase, (ii) the pyrrolnitrin biosynthesis operon, and (iii) the acdS gene encoding ACC deaminase; b) to employ these constructs to engineer stable recombinant strains with an expanded repertoire of beneficial activities; c) to evaluate the rhizosphere competence and antifungal activity of the WT and modified strains against pathogenic fungi under laboratory and greenhouse conditions; and d) to monitor the persistence and impact of the introduced strains on culturable and nonculturable rhizosphere microbial populations in the greenhouse and the field. The research generally support our concepts that combining strategically selected genes conferring diverse modes of action against plant pathogens into one organism can improve the efficacy of biological control agents. We hypothesized that biocontrol agents (BCAs) engineered to expand their repertoire of beneficial activities will more effectively control soilborne plant pathogens. In this work, we demonstrated that biocontrol activity of Pseudomonas fluorescens Q8r1-96 and Q2-87, both producing the antibiotic 2,4-diacetylphloroglucinol (2,4-DAPG) effective against the plant pathogenic fungus Rhizoctonia solani, can be improved significantly by introducing and expressing either the 1.6-kb gene chiA, encoding the 58-kDa endochitinase ChiA from the rhizosphere strain SerratiaplymuthicaIC1270, or the 5.8-kb prnABCDoperon encoding the broad-range antibiotic pyrrolnitrin (Prn) from another rhizosphere strain, P. fluorescens Pf-5. The PₜₐcchiAandPₜₐcprnABCDcassettes were cloned into the integrative pBK-miniTn7-ΩGm plasmid, and inserted into the genomic DNA of the recipient bacteria. Recombinant derivatives of strains Q8r1-96 and Q2-87 expressing the PₜₐcchiA or PₜₐcprnABCD cassettes produced endochitinase ChiA, or Prn, respectively, in addition to 2,4-DAPG, and the recombinants gave significantly better biocontrol of R. solani on beans under greenhouse conditions. The disease reduction index increased in comparison to the parental strains Q8r1-96 and Q2-87 to 17.5 and 39.0% from 3.2 and 12.4%, respectively, in the case of derivatives carrying the PₜₐcchiAcassette and to 63.1 and 70% vs. 2.8 and 12,4%, respectively, in the case of derivatives carrying the PₜₐcprnABCDcassette. The genetically modified strains exhibited persistence and non-target effects comparable to those of the parental strains in greenhouse soil. Three integrative cassettes carrying the acdS gene encoding ACC deaminase cloned under the control of different promoters were constructed and tested for enhancement of plant growth promotion by biocontrol strains of P. fluorescens and S. plymuthica. The integrative cassettes constructed in this work are already being used as a simple and efficient tool to improve biocontrol activity of various PGPR bacteria against fungi containing chitin in the cell walls or highly sensitive to Prn. Some parts of the work (e. g., construction of integrative cassettes) was collaborative while other parts e.g., (enzyme and antibiotic activity analyses) were fully synergistic. The US partners isolated and provided to the Israeli collaborators the original biocontrol strains P. fluorescens strains Q8r1-96 and Q2-87 and their mutants deficient in 2,4-DAPG production, which were used to evaluate the relative importance of introduction of Prn, chitinase or ACC deaminase genes for improvement of the biocontrol activity of the parental strains. The recombinant strains obtained at HUJI were supplied to the US collaborators for further analysis.
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Lifschitz, Eliezer, and Elliot Meyerowitz. The Relations between Cell Division and Cell Type Specification in Floral and Vegetative Meristems of Tomato and Arabidopsis. United States Department of Agriculture, February 1996. http://dx.doi.org/10.32747/1996.7613032.bard.

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Meristems were the central issue of our project. Genes that are required for cell division, cell elongation, cell proliferation and cell fate were studied in the tomato system. The analysis of the dUTPase and threonine deaminase genes, along with the dissection of their regulatory regions is completed, while that of the RNR2 and PPO genes is at an advanced stage. All these genes were isolated in our laboratory. In addition, 8 different MADS box genes were studied in transgenic plants and their genetic relevances discovered. We have also shown that a given MADS box gene can modify the polarity of cell division without affecting the fate of the organ. In vivo interaction between two MADS box genes was demonstrated and the functional dependency of the tomato agamous gene on the TM5 gene product established. We have exploited the Knotted1 meristematic gene in conjunction with tomato leaf meristematic genes to show that simple and compound leaves and, for that matter, sepals and compound leaves, are formed by two different developmental programs. In this context we have also isolated and characterized the tomato Knotted1 gene (TKnl) and studied its expression pattern. A new program in which eight different meristematic genes in tomato will be studied emerged as a result of these studies. In essence, we have shown that it is possible to study and manipulate plant developmental systems using reverse genetic techniques and have provided a wealth of new molecular tools to interested colleagues working with tomato. Similarly, genes responsible for cell division, cell proliferation and cell fate were studied in Arabidopsis floral meristems. Among these genes are the TSO1, TSO2, HANABA TARANU and UNUSUAL FLORAL ORGANS genes, each affecting in its own way the number of pattern of cell divisions, and cell fate, in developing Arabodopsis flowers. In addition, new methods have been established for the assessment of the function of regulatory gene action in the different clonal layers of developing floral meristems.
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Jander, Georg, Gad Galili, and Yair Shachar-Hill. Genetic, Genomic and Biochemical Analysis of Arabidopsis Threonine Aldolase and Associated Molecular and Metabolic Networks. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7696546.bard.

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Since the amino acids threonine and isoleucine can be limiting in mammalian diet and there is interest in increasing their abundance in certain crop plants. To meet this need, a BARD proposal was written with two main research objectives: (i) investigate new avenues for manipulating threonine and isoleucine content in plants and (ii) study the role of threonine aldolase in plant metabolism. Research conducted to meet these goals included analysis of the sub-cellular localization of threonine aldolase in the plant, analysis of metabolic flux in developing embryos, over- and under-expression of Arabidopsis threonine aldolases, and transcriptional and metabolic analysis of perturbations resulting from altered threonine aldolase expression. Additionally, the broader metabolic effects of increasing lysine biosynthesis were investigated. An interesting observation that came up in the course of the project is that threonine aldolase activity affects methionine gamma-lyase in Arabidopsis. Further research showed that threonine deaminase and methionine gamma-lyase both contribute to isoleucine biosynthesis in plants. Therefore, isoleucine content can be altered by manipulating the expression of either or both of these enzymes. Additionally, both enzymes contribute to the up to 100-fold increase in isoleucine that is observed in drought-stressed Arabidopsis. Toward the end of the project it was discovered that through different projects, both groups had been able to independently up-regulate phenylalanine accumulation by different mechanisms. The Galili lab transformed Arabidopsis with a feedbackinsensitive bacterial enzyme and the Jander lab found a feedback insensitive mutation in Arabidopsis arogenate dehydratase. Exchange of the respective plant lines has allowed a comparative analysis of the different methods for increasing phenylalanine content and the creation of double mutants. The research that was conducted as part of this BARD project has led to new insights into plant amino acid metabolism. Additionally, new approaches that were found to increase the accumulation of threonine, isoleucine, and phenylalanine in plants have potential practical applications. Increased threonine and isoleucine levels can increase the nutritional value of crop plants. Elevated isoleucine accumulation may increase the osmotic stress tolerance of plants. Up-regulation of phenylalanine biosynthesis can be used to increase the production of downstream higher-value plant metabolites of biofuel feed stocks.
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