Academic literature on the topic 'Endonucleasi'

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Journal articles on the topic "Endonucleasi"

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Fahmi, Tariq, Xiaoying Wang, Dmitry D. Zhdanov, Intisar Islam, Eugene O. Apostolov, Alena V. Savenka, and Alexei G. Basnakian. "DNase I Induces Other Endonucleases in Kidney Tubular Epithelial Cells by Its DNA-Degrading Activity." International Journal of Molecular Sciences 21, no. 22 (November 17, 2020): 8665. http://dx.doi.org/10.3390/ijms21228665.

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Endonuclease-mediated DNA fragmentation is both an immediate cause and a result of apoptosis and of all other types of irreversible cell death after injury. It is produced by nine enzymes including DNase I, DNase 2, their homologs, caspase-activated DNase (CAD) and endonuclease G (EndoG). The endonucleases act simultaneously during cell death; however, regulatory links between these enzymes have not been established. We hypothesized that DNase I, the most abundant of endonucleases, may regulate other endonucleases. To test this hypothesis, rat kidney tubular epithelial NRK-52E cells were transfected with the DNase I gene or its inactive mutant in a pECFP expression vector, while control cells were transfected with the empty vector. mRNA expression of all nine endonucleases was studied using real-time RT-PCR; DNA strand breaks in endonuclease genes were determined by PCR and protein expression of the enzymes was measured by Western blotting and quantitative immunocytochemistry. Our data showed that DNase I, but not its inactive mutant, induces all other endonucleases at varying time periods after transfection, causes DNA breaks in endonuclease genes, and elevates protein expression of several endonucleases. This is the first evidence that endonucleases seem to be induced by the DNA-degrading activity of DNase I.
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Kamisugi, Y., Y. Ikeda, M. Ohno, M. Minezawa, and K. Fukui. "In situ digestion of barley chromosomes with restriction endonucleases." Genome 35, no. 5 (October 1, 1992): 793–98. http://dx.doi.org/10.1139/g92-121.

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In situ digestion of barley chromosomes with restriction endonucleases was examined. All the treatments with five restriction endonucleases, MboII, RsaI, HaeIII, HinfI, and DraII, showed various band patterns on the barley chromosomes. Differences were observed in the band patterns produced with different restriction endonucleases. Uneven staining patterns, similar to the band patterns by the endonuclease treatments, also appeared when the chromosomes were treated with the buffer solution without the enzyme. The band patterns observed both with and without the endonucleases were classified into the four types and the frequency of each type among the different treatments was investigated. The change of the band types along with treatment time was accelerated by the addition of the restriction endonuclease. As a result, it was concluded that there existed chromosome band patterns that were specific to the endonuclease treatments and that the buffer solution also affected to the production of the bands on the chromosomes.Key words: Hordeum vulgare L., chromosome band pattern, in situ digestion, restriction endonuclease, restriction banding.
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Petersen, Kamilla Vandsø, Cinzia Tesauro, Marianne Smedegaard Hede, Camilla Pages, Lærke Bay Marcussen, Josephine Geertsen Keller, Magnus Bugge, et al. "Rolling Circle Enhanced Detection of Specific Restriction Endonuclease Activities in Crude Cell Extracts." Sensors 22, no. 20 (October 13, 2022): 7763. http://dx.doi.org/10.3390/s22207763.

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Restriction endonucleases are expressed in all bacteria investigated so far and play an essential role for the bacterial defense against viral infections. Besides their important biological role, restriction endonucleases are of great use for different biotechnological purposes and are indispensable for many cloning and sequencing procedures. Methods for specific detection of restriction endonuclease activities can therefore find broad use for many purposes. In the current study, we demonstrate proof-of-concept for a new principle for the detection of restriction endonuclease activities. The method is based on rolling circle amplification of circular DNA products that can only be formed upon restriction digestion of specially designed DNA substrates. By combining the activity of the target restriction endonuclease with the highly specific Cre recombinase to generate DNA circles, we demonstrate specific detection of selected restriction endonuclease activities even in crude cell extracts. This is, to our knowledge, the first example of a sensor system that allows activity measurements of restriction endonucleases in crude samples. The presented sensor system may prove valuable for future characterization of bacteria species or strains based on their expression of restriction endonucleases as well as for quantification of restriction endonuclease activities directly in extracts from recombinant cells.
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Shammas, Masood A., Hemant Koley, Sima Shah, Ramesh B. Batchu, Pierfrancesco Tassone, Kenneth C. Anderson, and Nikhil C. Munshi. "Dysregulated Apurinic/Apyrimidinic Endonucleases (Ape1 and Ape2) Lead to Genetic Instability in Multiple Myeloma." Blood 104, no. 11 (November 16, 2004): 1418. http://dx.doi.org/10.1182/blood.v104.11.1418.1418.

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Abstract Multiple myeloma (MM) is associated with significant genomic instability. Homologous recombination (HR), which is elevated in MM, is considered to be responsible for this instability. As endonucleases play an important role in mediating HR, here we have evaluated the role of endonuclease in biology and progression of MM. Gene expression profile using Affymetrix U133 array showed > 2 fold elevation of Ape1 or Ape2 or both in 5 of 6 MM cell lines and 12 of 15 patient samples. Immunocytochemistry confirmed upregulation of Ape1 protein in MM cell lines. A Plasmid degradation assay confirmed significantly elevated endonuclease activity in MM cells compared to normal plasma cells. To identify the pre-dominating endonuclease activity, the degradation assay was carried out in the presence of specific endonuclease inhibitors. Harmane and methoxyamine (MA), specific inhibitors of apurinic/apyrimidinic endonucleases effectively inhibited significant endonuclease activity, while other endonuclease inhibitors ACPD and FK506 had minimal effects, confirming predominant role of apurinic/apyrimidinic endonucleases (APE) in mediating increased endonuclease activity in MM. We investigated the role of elevated APE endonuclease activity on DNA recombination and subsequent genomic re-arrangements. Using a plasmid-based assay we have previously demonstrated significantly elevated homologous recombination (HR) in MM. Inhibition of endonuclease by methoxyamine suppressed HR activity by 85 ± 2% in MM cells. Next, we evaluated whether inhibition of HR by methoxyamine can affect the frequency of acquisition of new genetic changes in MM cells using single nucleotide polymorphism (SNP) arrays (Affymetrix) as indicator of genomic instability. In three independent experiments, methoxyamine reduced the acquisition of new loss of heterozygocity (LOH) loci by an average of 71%. These data suggest that the dysregulated APE endonucleases contribute significantly to the genomic instability, acquisition of new mutations and progression of MM and provides the rationale for targeting endonuclease activity to prevent disease progression including development of drug resistance.
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Landthaler, Markus, Nelson C. Lau, and David A. Shub. "Group I Intron Homing in Bacillus Phages SPO1 and SP82: a Gene Conversion Event Initiated by a Nicking Homing Endonuclease." Journal of Bacteriology 186, no. 13 (July 1, 2004): 4307–14. http://dx.doi.org/10.1128/jb.186.13.4307-4314.2004.

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ABSTRACT Many group I introns encode endonucleases that promote intron homing by initiating a double-stranded break-mediated homologous recombination event. In this work we describe intron homing in Bacillus subtilis phages SPO1 and SP82. The introns encode the DNA endonucleases I-HmuI and I-HmuII, respectively, which belong to the H-N-H endonuclease family and possess nicking activity in vitro. Coinfections of B. subtilis with intron-minus and intron-plus phages indicate that I-HmuI and I-HmuII are required for homing of the SPO1 and SP82 introns, respectively. The homing process is a gene conversion event that does not require the major B. subtilis recombination pathways, suggesting that the necessary functions are provided by phage-encoded factors. Our results provide the first examples of H-N-H endonuclease-mediated intron homing and the first demonstration of intron homing initiated by a nicking endonuclease.
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GRISHIN, ALEXANDER, INES FONFARA, ANDREI ALEXEEVSKI, SERGEI SPIRIN, OLGA ZANEGINA, ANNA KARYAGINA, DANIIL ALEXEYEVSKY, and WOLFGANG WENDE. "IDENTIFICATION OF CONSERVED FEATURES OF LAGLIDADG HOMING ENDONUCLEASES." Journal of Bioinformatics and Computational Biology 08, no. 03 (June 2010): 453–69. http://dx.doi.org/10.1142/s0219720010004665.

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LAGLIDADG family of homing endonucleases are rare-cutting enzymes which recognize long target sequences and are of great interest in genome engineering. Despite advances in homing endonuclease engineering, effective methods of broadening the range of cleaved sequences are still lacking. Here, we present a study of conserved structural features of LAGLIDADG homing endonucleases that might aid further development of such methods. The protein–DNA interface of LAGLIDADG homing endonucleases differs considerably with the particular nuclease, and the analysis of conserved protein–DNA interactions could not identify any residues crucial for DNA binding and common to most nucleases of the family. For the homing endonuclease PI-SceI, a comparison of structural and experimental data derived from literature helped to identify 23 residues that are likely to be important for DNA binding. Analysis of the LAGLIDADG domain dimerization interface allowed the choosing of six positions that contribute to dimerization specificity most, while comparison of 446 sequences of LAGLIDADG endonucleases revealed groups of residues in these positions that appear to be most favorable for dimerization.
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Everett, Blake A., Lauren A. Litzau, Kassidy Tompkins, Ke Shi, Andrew Nelson, Hideki Aihara, Robert L. Evans, and Wendy R. Gordon. "Crystal structure of the Wheat dwarf virus Rep domain." Acta Crystallographica Section F Structural Biology Communications 75, no. 12 (November 27, 2019): 744–49. http://dx.doi.org/10.1107/s2053230x19015796.

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The Rep domain of Wheat dwarf virus (WDV Rep) is an HUH endonuclease involved in rolling-circle replication. HUH endonucleases coordinate a metal ion to enable the nicking of a specific ssDNA sequence and the subsequent formation of an intermediate phosphotyrosine bond. This covalent protein–ssDNA adduct makes HUH endonucleases attractive fusion tags (HUH-tags) in a diverse number of biotechnological applications. Solving the structure of an HUH endonuclease in complex with ssDNA will provide critical information about ssDNA recognition and sequence specificity, thus enabling rationally engineered protein–DNA interactions that are programmable. The structure of the WDV Rep domain reported here was solved in the apo state from a crystal diffracting to 1.24 Å resolution and represents an initial step in the direction of solving the structure of a protein–ssDNA complex.
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Bultmann, H., and R. Mezzanotte. "Characterization and origin of extrachromosomal DNA granules in Sarcophaga bullata." Journal of Cell Science 88, no. 3 (October 1, 1987): 327–34. http://dx.doi.org/10.1242/jcs.88.3.327.

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We have used endonuclease treatment in situ, followed by Giemsa or ethidium bromide staining, for mapping repetitive sequences on the chromosomes of the flesh fly Sarcophaga bullata and thus for studying extrachromosomal DNA granules in this species. All three restriction enzymes employed (HaeIII, A1uI and HindIII) show the same cytological effects, except for a single interstitial band. In both polytene and mitotic chromosomes, chromatin resistant to these endonucleases presumably includes at least three endonucleases presumably includes at least three previously unrecognized buoyant density satellites (1.663, 1.670 and 1.692 g ml-1 in neutral CsCl), and is predominantly localized in the pericentric regions of all five autosomes. Mitotic treated chromosomes show that the entire rod-shaped X chromosome, but no part of the dot-like Y chromosome, consists of endonuclease-resistant chromatin. The most unusual heterochromatic component of polytene nuclei in this species, the ‘extrachromosomal DNA granules’, are also entirely resistant to digestion with endonucleases. We think that these DNA granules represent dispersed X chromatin and not, as previously assumed, extruded autosomal heterochromatin.
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Jordano-Raya, Marina, Cristina Beltrán-Melero, M. Dolores Moreno-Recio, M. Isabel Martínez-Macías, Rafael R. Ariza, Teresa Roldán-Arjona, and Dolores Córdoba-Cañero. "Complementary Functions of Plant AP Endonucleases and AP Lyases during DNA Repair of Abasic Sites Arising from C:G Base Pairs." International Journal of Molecular Sciences 22, no. 16 (August 16, 2021): 8763. http://dx.doi.org/10.3390/ijms22168763.

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Abasic (apurinic/apyrimidinic, AP) sites are ubiquitous DNA lesions arising from spontaneous base loss and excision of damaged bases. They may be processed either by AP endonucleases or AP lyases, but the relative roles of these two classes of enzymes are not well understood. We hypothesized that endonucleases and lyases may be differentially influenced by the sequence surrounding the AP site and/or the identity of the orphan base. To test this idea, we analysed the activity of plant and human AP endonucleases and AP lyases on DNA substrates containing an abasic site opposite either G or C in different sequence contexts. AP sites opposite G are common intermediates during the repair of deaminated cytosines, whereas AP sites opposite C frequently arise from oxidized guanines. We found that the major Arabidopsis AP endonuclease (ARP) exhibited a higher efficiency on AP sites opposite G. In contrast, the main plant AP lyase (FPG) showed a greater preference for AP sites opposite C. The major human AP endonuclease (APE1) preferred G as the orphan base, but only in some sequence contexts. We propose that plant AP endonucleases and AP lyases play complementary DNA repair functions on abasic sites arising at C:G pairs, neutralizing the potential mutagenic consequences of C deamination and G oxidation, respectively.
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Carnes, Jason, Carmen Zelaya Soares, Carey Wickham, and Kenneth Stuart. "Endonuclease Associations with Three Distinct Editosomes in Trypanosoma brucei." Journal of Biological Chemistry 286, no. 22 (April 7, 2011): 19320–30. http://dx.doi.org/10.1074/jbc.m111.228965.

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Three distinct editosomes, typified by mutually exclusive KREN1, KREN2, or KREN3 endonucleases, are essential for mitochondrial RNA editing in Trypanosoma brucei. The three editosomes differ in substrate endoribonucleolytic cleavage specificity, which may reflect the vast number of editing sites that need insertion or deletion of uridine nucleotides (Us). Each editosome requires the single RNase III domain in each endonuclease for catalysis. Studies reported here show that the editing endonucleases do not form homodimeric domains, and may therefore function as intermolecular heterodimers, perhaps with KREPB4 and/or KREPB5. Editosomes isolated via TAP tag fused to KREPB6, KREPB7, or KREPB8 have a common set of 12 proteins. In addition, KREN3 is only found in KREPB6 editosomes, KREN2 is only found in KREPB7 editosomes, and KREN1 is only found in KREPB8 editosomes. These are the same associations previously found in editosomes isolated via the TAP-tagged endonucleases KREN1, KREN2, or KREN3. Furthermore, TAP-tagged KREPB6, KREPB7, and KREPB8 complexes isolated from cells in which expression of their respective endonuclease were knocked down were disrupted and lacked the heterotrimeric insertion subcomplex (KRET2, KREPA1, and KREL2). These results and published data suggest that KREPB6, KREPB7, and KREPB8 associate with the deletion subcomplex, whereas the KREN1, KREN2, and KREN3 endonucleases associate with the insertion subcomplex.
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Dissertations / Theses on the topic "Endonucleasi"

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FIRRITO, CLAUDIA. "Targeted Gene Correction and Reprogramming of SCID-X1 Fibroblasts to Rescue IL2RG Expression in iPSC-derived Hematopoietic Cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/94656.

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La terapia genica basata sull’utilizzo di vettori integranti è stata già applicata con successo per la cura di varie malattie genetiche come le malattie da accumulo lisosomiale (LSD), la beta-talassemia (β-Thal) e le immunodeficienze primarie (PID). L’immunodeficienza combinata grave legata al cromosoma X (SCID-X1) è una malattia monogenica letale causata da mutazioni del gene codificante la catena comune gamma del recettore per l’interleuchina 2 (IL2RG). I primi studi clinici per la SCID-X1 hanno mostrato il potenziale terapeutico della terapia genica basata su vettori integranti, risultando nella ricostituzione del compartimento linfoide grazie al vantaggio selettivo delle cellule geneticamente modificate. D’altra parte, tali studi hanno evidenziato il rischio di mutagenesi inserzionale dovuto all’integrazione casuale del virus nel genoma della cellula ospite e all’espressione non regolata del transgene, sottolineando la necessità di sviluppare nuove strategie di terapia genica più sicure. In questo lavoro, sfruttando la tecnologia delle Zinc-Finger Nucleasi (ZFN) per indurre una rottura del doppio filamento del DNA in maniera sito specifica e dei vettori lentivirali difettivi per l’integrazione (IDLV) per l’introduzione di un templato donatore, abbiamo impiegato il processo di riparazione del DNA guidata dall’omologia per la correzione delle mutazioni che causano la SCID-X1, ripristinando così la funzione genica e l’espressione fisiologica del gene IL2RG. Mediante l’integrazione di un cDNA correttivo del gene IL2RG a valle del promotore endogeno sia in cellule B linfoblastodi, che esprimono costitutivamente la catena gamma comune, sia in linfociti T da donatori sani, che richiedono IL2RG per la loro sopravvivenza, abbiamo dimostrato la funzionalità e l’attività fisiologica del gene modificato. Abbiamo quindi accoppiato la correzione genica con la selezione delle cellule mediante l’inclusione di una cassetta excidibile di espressione della GFP o della resistenza alla puromicina (PuroR) a valle del cDNA correttivo, al fine di correggere fibroblasti, che normalmente non esprimono IL2R, derivati da pazienti SCID-X1. Abbiamo quindi ottenuto una popolazione di fibroblasti corretti che abbiamo “ riprogrammato” mediante un nuovo vettore di reprogramming che esprime i fattori di trascrizione (SOX2, OCT4, KLf4) e il microRNA cluster 367, generando così una fonte illimitata di cellule staminali pluripotenti indotte (iPSC) geneticamente corrette di interesse terapeutico. L’espressione transiente della Cre-ricombinasi mediante IDLV ha inoltre permesso l’excisione del vettore di reprogramming e della cassetta di selezione, permettendo così l’ottenimento di cellule iPSC corrette, prive di vettore e con un normale cariotipo. Infine, attraverso il differenziamento delle cellule iPSC in progenitori T-linfoidi, un tipo cellulare assente nei pazienti SCID-X1, e l’osservazione di un vantaggio selettivo delle cellule linfoidi derivate dalle iPSC corrette, abbiamo dimostrato la correzione funzionale dell’allele IL2RG mutato. In conclusione questi dati dimostrano la validità della nostra strategia di integrazione sito-specifica che, mediante la correzione e la riprogrammazione cellulare, consente di ottenere cellule iPSC geneticamente corrette, aprendo la strada a nuove opportunità terapeutiche più sicure per il trattamento della SCID-X1.
Gene replacement by integrating vectors has been successfully used to treat several inherited diseases, such as Lysosomal Storage Disorders (LSD), Thalassemia and Primary Immunodeficiencies (PIDs). X-linked Combined Immunodeficiency (SCID-X1) is a fatal monogenic disorder, caused by mutation of the Interleukin 2 Receptor common γ-chain (IL2RG) gene. For SCID-X1, the early clinical studies have clearly shown the therapeutic potential of integrating vector based gene replacement therapy, which achieved efficient lymphoid reconstitution thanks to the selective growth advantage of the genetically modified cells. However, these studies also highlighted the potential risk of insertional mutagenesis due to random integration of the vector into the host cell genome and to unregulated transgene expression, thus calling for the development of safer gene therapy approaches. Here, by combining the Zinc Finger Nuclease (ZFNs) technology to induce site-specific DNA double-strand breaks (DSB) and of Integrase-Defective Lentiviral Vector (IDLV) to deliver a corrective donor template, we exploited Homology Driven Repair (HDR) to correct SCID-X1 mutation in situ, restoring both physiological expression and function of the IL2RG gene . By knocking-in a corrective IL2RG cDNA transgene downstream of its endogenous promoter in B-lymphoblastoid cells, which constitutively express IL2RG, and in primary T-lymphocytes, which requires IL2RG for their survival and growth, we provide evidence of physiologic activity of the gene-edited IL2RG gene. By including an excisable GFP- or a Puromycin Resistance (PuroR) expression cassette downstream of the corrective cDNA, we coupled correction with exogenous selection of corrected SCID-X1 primary fibroblasts, which do not physiologically express IL2RG, and obtained an enriched population of gene-corrected cells. We then reverted this population to pluripotency by using a novel reprogramming vector that expresses OCT4, SOX2, KLF4 and microRNA cluster 302-367 to obtain a potentially unlimited source of gene-corrected induced pluripotent stem cells (iPSC). We thus generated several gene-corrected bona-fide iPSCs, as confirmed by molecular analyses for targeted integration, which were characterized for their pluripotent state. IDLV-mediated transient delivery of the Cre-recombinase resulted in the co-excision of the reprogramming vector together with the selector cassette, thus allowing the generation of several gene-corrected, reprogramming-factor free iPSCs with normal karyotypes. Finally, by differentiating corrected iPSC to T-lymphoid progenitor cells, which are lacking in SCID-X1 patients, and showing a selective growth advantage of those derived from corrected iPSCs, we provide evidence of the functional correction of the IL2RG mutant allele. Overall these data demonstrate the feasibility of our targeted gene editing strategy, which couples gene correction with cell reprogramming to generate disease-free IPSC, thus paving the way for the development of novel and safer therapeutic approaches for SCID-X1.
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Daniels, Lucy Elizabeth. "The SgrAI restriction endonuclease." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393877.

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Chevalier, Brett S. "Homing endonuclease mechanism, structure and design /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/4984.

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AlMalki, Faizah. "Structural studies on flap endonuclease complexes." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/7293/.

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Flap endonucleases (FENs) are structure-specific enzymes that play critical roles in DNA replication and repair. Three members of the FEN family have been investigated during this project in complexes with DNA substrates and metal ions: bacteriophage T5FEN, hFEN and Trypanosoma brucei FEN. T5FEN wild type and two catalytically inactive versions, D153K and D155K were successfully crystallized in complexes with DNA substrates containing 5' or 3' overhangs. The crystal structure for T5FEN-D153K in complex with a duplex containing 5' overhangs at each end and two Mg2+ ions was solved. The structure of T5FEN-D155K was solved in complex with a duplex containing 3' overhangs and a Ca2+ ion in the active site. In addition, wild type T5FEN was also crystallized with the same 3'-overhang substrate in the absence of metal ions. These structures revealed that the single strand-5' overhang in T5FEN-D153K pushed electrostatically and looped-up before threading through an arch-like structure composed of two helixes located over the active site of the enzyme. This arch is fully ordered in all of these structures. In the active sites of the variant complexes the Lys-153 and Lys155 are visible. The lysine's long side chain allows its ε amino group to occupy similar positions to the metal ion sites in one of the two active site subsites known as Cat1. The ε amino of Lys-153 directly coordinates the scissile phosphate of the DNA substrate. Important residues concerned with the 5' overhang threading are also determined. His-36 rotates by 180° to allow the duplex DNA movement before threading while Tyr-90 and Phe-105 form a gate-like structure after the 5' overhang has threaded. The conserved Arg-86 plays a critical role in 5' overhang transmission during threading process. Lys-83 and Arg-125 are found to interact symmetrically with the DNA backbone in the T5FEN-D155K:DNA complex. A new trans-arch/distal phosphate-binding site composed of Gly- 70 and Lys-71 has been determined in the far side of the arch. These structures of T5FEN also have a binding site for the potassium ion within the H3TH motif coordinated by the main chain carbonyl oxygens of three residues and directly interacted with the DNA phosphate group.
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Barzilay, Gil. "Characterisation of human AP endonuclease I (HAP1)." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318791.

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Pernstich, Christian. "Protein dynamics of the restriction endonuclease Fokl." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526007.

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Stanford, Neil Philip. "DNA cleavage by the EcoRV restriction endonuclease." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299311.

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Wentzell, Lois Marie. "DNA communications by the SfiI restriction endonuclease." Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388002.

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Hanson, Mark Nils. "Biochemical characterization of the endonuclease PMR-1 /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488204276532461.

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Zhao, Lei. "Characterization of bacterial homing endonuclease I-Ssp6803I /." Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/9214.

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Books on the topic "Endonucleasi"

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Edgell, David R., ed. Homing Endonucleases. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-968-0.

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Pingoud, Alfred M., ed. Restriction Endonucleases. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0.

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Homing endonucleases: Methods and protocols. New York: Humana Press, 2014.

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Belfort, Marlene, David W. Wood, Barry L. Stoddard, and Victoria Derbyshire, eds. Homing Endonucleases and Inteins. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-29474-0.

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G, Chirikjian Jack, ed. Restriction endonucleases and methylases. New York: Elsevier, 1987.

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Bolton, Bryan John. Class ii restriction endonucleases: Screening, purification and characterization. Salford: University of Salford, 1988.

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Cross, Stephen R. H. Restriction endonuclease map variation and natural selection in populations of Drosophila melanogaster. Birmingham: University of Birmingham, 1985.

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Price, Rebecca Clare. The effects of restriction endonucleases on mammalian cells of different radiosensitivity. Manchester: University of Manchester, 1994.

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Fraser, Murray J. Endo-exonucleases. Austin, Tex: R.G. Landes Co., 1996.

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Cartwright, Nicola. Detection and typing of human papillomavirus using semi-nested PCR and restriction endonuclease analysis with respect to vulval carcinoma. [s.l.]: typescript, 1996.

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Book chapters on the topic "Endonucleasi"

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Gooch, Jan W. "Endonuclease." In Encyclopedic Dictionary of Polymers, 889. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13647.

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Sugiyama, Munetaka, Jun Ito, Shigemi Aoyagi, and Hiroo Fukuda. "Endonucleases." In Programmed Cell Death in Higher Plants, 143–53. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-010-0934-8_11.

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Roberts, R. J., M. Belfort, T. Bestor, A. S. Bhagwat, T. A. Bickle, J. Bitinaite, R. M. Blumenthal, et al. "A Nomenclature for Restriction Enzymes, DNA Methyltransferases, Homing Endonucleases, and Their Genes." In Restriction Endonucleases, 1–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_1.

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Reuter, M., M. Mücke, and D. H. Krüger. "Structure and Function of Type IIE Restriction Endonucleases — or: From a Plasmid That Restricts Phage Replication to A New Molecular DNA Recognition Mechanism." In Restriction Endonucleases, 261–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_10.

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Welsh, A. J., S. E. Halford, and D. J. Scott. "Analysis of Type II Restriction Endonucleases that Interact with Two Recognition Sites." In Restriction Endonucleases, 297–317. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_11.

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Sidorova, N., and D. C. Rau. "The Role of Water in the EcoRI-DNA Binding." In Restriction Endonucleases, 319–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_12.

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Cowan, J. A. "Role of Metal Ions in Promoting DNA Binding and Cleavage by Restriction Endonucleases." In Restriction Endonucleases, 339–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_13.

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Horton, J. R., R. M. Blumenthal, and X. Cheng. "Restriction Endonucleases: Structure of the Conserved Catalytic Core and the Role of Metal Ions in DNA Cleavage." In Restriction Endonucleases, 361–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_14.

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Alves, J., and P. Vennekohl. "Protein Engineering of Restriction Enzymes." In Restriction Endonucleases, 393–411. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_15.

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Kandavelou, K., M. Mani, S. Durai, and S. Chandrasegaran. "Engineering and Applications of Chimeric Nucleases." In Restriction Endonucleases, 413–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_16.

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Conference papers on the topic "Endonucleasi"

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"Comparison of the conformational dynamics of structurally different AP-endonucleases APE1 and Nfo during AP-endonuclease activity." In Systems Biology and Bioinformatics (SBB-2021) : The 13th International Young Scientists School;. ICG SB RAS, 2021. http://dx.doi.org/10.18699/sbb-plantgen-2021-16.

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Orlovskaya, P. I., T. A. Pilipchuk, N. I. Girilovich, M. N. Mandrik-Litvinkovich, and E. I. Kalamiyets. "Investigation of genetic heterogeneity of phages from phytopathogenic bacteria Xanthomonas phaseoli." In 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.188.

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Kitajima, Tsubasa, Akira Hirata, Chikako Iwashita, Shin-ichi Yokobori, and Hiroyuki Hori. "Enzymatic and crystallographic characterization of archaeal tRNA splicing endonuclease." In 2009 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2009. http://dx.doi.org/10.1109/mhs.2009.5352027.

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Topka, Sabine, Sara Kazzaz, Kenneth Offit, and Vijai Joseph. "Abstract 5367: Ngago: no evidence of targeted endonuclease activity." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5367.

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Wang, Yuejun, Yihong Qiu, Zhende Huang, and Zhu Yisheng. "Modelling on the Kinetics Mechanism of the FokI Restriction Endonuclease." In 2007 1st International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/icbbe.2007.6.

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"Generation of haploidy inducers for Cas endonuclease-mediated mutagenesis in barley." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Novosibirsk ICG SB RAS 2021, 2021. http://dx.doi.org/10.18699/plantgen2021-178.

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Mačková, Michaela, and Michal Hocek. "Vinyl-modified DNA and its cleavage by restriction endonucleases." In XVIth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2014. http://dx.doi.org/10.1135/css201414318.

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"Structural features of substrate recognition by APE1-like endonucleases." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-570.

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Hazarika, Zaved, and Anupam Nath Jha. "A Comparative Evaluation of Docking Programs using Influenza Endonuclease as Target Protein." In 2020 International Conference on Computational Performance Evaluation (ComPE). IEEE, 2020. http://dx.doi.org/10.1109/compe49325.2020.9200180.

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Liao, Huang-Sheng, Josephine W. Wu, Hsuan-Liang Liu, Jian-Hua Zhao, Kung-Tien Liu, Chih-Kuang Chuang, Hsin-Yi Lin, Wei-Bor Tsai, and Yih Ho. "Pharmacophore and Virtual Screening to Design the Potential Influenza Virus Endonuclease Inhibitors." In 14th Asia Pacific Confederation of Chemical Engineering Congress. Singapore: Research Publishing Services, 2012. http://dx.doi.org/10.3850/978-981-07-1445-1_327.

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Reports on the topic "Endonucleasi"

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Yeung, Anthony T. Detection of Mutations Using a Novel Endonuclease. Fort Belvoir, VA: Defense Technical Information Center, June 1998. http://dx.doi.org/10.21236/adb238444.

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Lue, Neal F. Structural and Functional Characterization of a Telomerase-Associated Endonuclease. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada411390.

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Lue, Neal F. Structural and Functional Characterization of a Telomerase-Associated Endonuclease. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada417028.

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Feigon, Juli. Recognition of DNA by EcoRI Restriction Endonuclease and Methylase. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada247626.

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Braun, W. A. Molecular Recognition of DNA Damage Sites by Apurinic/Apyrimidinic Endonucleases. Office of Scientific and Technical Information (OSTI), July 2005. http://dx.doi.org/10.2172/877152.

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Knoche, K., S. Selman, and L. Hung. Site specific endonucleases for human genome mapping. Final report, April 1, 1992--March 31, 1994. Office of Scientific and Technical Information (OSTI), June 1994. http://dx.doi.org/10.2172/188888.

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Wilson, Thomas E., Avraham A. Levy, and Tzvi Tzfira. Controlling Early Stages of DNA Repair for Gene-targeting Enhancement in Plants. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7697124.bard.

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Abstract:
Gene targeting (GT) is a much needed technology as a tool for plant research and for the precise engineering of crop species. Recent advances in this field have shown that the presence of a DNA double-strand break (DSB) in a genomic locus is critical for the integration of an exogenous DNA molecule introduced into this locus. This integration can occur via either non-homologous end joining (NHEJ) into the break or homologous recombination (HR) between the broken genomic DNA and the introduced vector. A bottleneck for DNA integration via HR is the machinery responsible for homology search and strand invasion. Important proteins in this pathway are Rad51, Rad52 and Rad54. We proposed to combine our respective expertise: on the US side, in the design of zincfinger nucleases (ZFNs) for the induction of DNA DSBs at any desired genomic locus and in the integration of DNA molecules via NHEJ; and on the Israeli side in the HR events, downstream of the DSB, that lead to homology search and strand invasion. We sought to test three major pathways of targeted DNA integration: (i) integration by NHEJ into DSBs induced at desired sites by specially designed ZFNs; (ii) integration into DSBs induced at desired sites combined with the use of Rad51, Rad52 and Rad54 proteins to maximize the chances for efficient and precise HR-mediated vector insertion; (iii) stimulation of HR by Rad51, Rad52 and Rad54 in the absence of DSB induction. We also proposed to study the formation of dsT-DNA molecules during the transformation of plant cells. dsT-DNA molecules are an important substrate for HR and NHEJ-mediatedGT, yet the mode of their formation from single stranded T-DNA molecules is still obscure. In addition we sought to develop a system for assembly of multi-transgene binary vectors by using ZFNs. The latter may facilitate the production of binary vectors that may be ready for genome editing in transgenic plants. ZFNs were proposed for the induction of DSBs in genomic targets, namely, the FtsH2 gene whose loss of function can easily be identified in somatic tissues as white sectors, and the Cruciferin locus whose targeting by a GFP or RFP reporter vectors can give rise to fluorescent seeds. ZFNs were also proposed for the induction of DSBs in artificial targets and for assembly of multi-gene vectors. We finally sought to address two important cell types in terms of relevance to plant transformation, namely GT of germinal (egg) cells by floral dipping, and GT in somatic cells by root and leave transformation. To be successful, we made use of novel optimized expression cassettes that enable coexpression of all of the genes of interest (ZFNs and Rad genes) in the right tissues (egg or root cells) at the right time, namely when the GT vector is delivered into the cells. Methods were proposed for investigating the complementation of T-strands to dsDNA molecules in living plant cells. During the course of this research, we (i) designed, assembled and tested, in vitro, a pair of new ZFNs capable of targeting the Cruciferin gene, (ii) produced transgenic plants which expresses for ZFN monomers for targeting of the FtsH2 gene. Expression of these enzymes is controlled by constitutive or heat shock induced promoters, (iii) produced a large population of transgenic Arabidopsis lines in which mutated mGUS gene was incorporated into different genomic locations, (iv) designed a system for egg-cell-specific expression of ZFNs and RAD genes and initiate GT experiments, (v) demonstrated that we can achieve NHEJ-mediated gene replacement in plant cells (vi) developed a system for ZFN and homing endonuclease-mediated assembly of multigene plant transformation vectors and (vii) explored the mechanism of dsTDNA formation in plant cells. This work has substantially advanced our understanding of the mechanisms of DNA integration into plants and furthered the development of important new tools for GT in plants.
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