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Ligase IV

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https://www.readbyqxmd.com/read/28577191/deletion-analysis-of-gh7-endoglucanase-gene-cel7b-promoter-region-in-a-talaromyces-cellulolyticus-ligd-disrupted-strain
#1
Tatsuya Fujii, Hiroyuki Inoue, Kazuhiko Ishikawa, Tamotsu Hoshino
Talaromyces cellulolyticus is expected to become an industrial cellulase producer. In this study, we performed deletion analysis of the promoter region of the GH7 endoglucanase gene (cel7B), which encodes one of the major cellulases, using a β-glucuronidase reporter system. To obtain strains that harbor each gene cassette at the same locus, we had to improve the homologous recombination frequency. Hence, the ligD gene, encoding DNA ligase IV, was disrupted by homologous recombination. After that, the introduced pyrF marker gene, encoding orotate phosphoribosyl transferase, was deleted by a marker recycling system...
June 2, 2017: Applied Biochemistry and Biotechnology
https://www.readbyqxmd.com/read/28392333/outcome-of-hematopoietic-cell-transplantation-for-dna-double-strand-breakage-repair-disorders
#2
James Slack, Michael H Albert, Dmitry Balashov, Bernd H Belohradsky, Alice Bertaina, Jack Bleesing, Claire Booth, Jochen Büchner, Rebecca H Buckley, Marie Ouachée-Chardin, Elena Deripapa, Katarzyna Drabko, Mary Eapen, Tobias Feuchtinger, Andrea Finocchi, H Bobby Gaspar, Sujal Ghosh, Alfred Gillio, Luis I Gonzalez-Granado, Eyal Grunebaum, Tayfun Güngör, Carsten Heilmann, Merja Helminen, Kohei Higuchi, Kohsuke Imai, Krzysztof Kalwak, Nubuo Kanazawa, Gülsün Karasu, Zeynep Y Kucuk, Alexandra Laberko, Andrzej Lange, Nizar Mahlaoui, Roland Meisel, D Moshous, Hideki Muramatsu, Suhag Parikh, Srdjan Pasic, Irene Schmid, Catharina Schuetz, Ansgar Schulz, Kirk R Schultz, Peter J Shaw, Mary A Slatter, Karl-Walter Sykora, Shinobu Tamura, Mervi Taskinen, Angela Wawer, Beata Wolska-Kus Nierz, Morton J Cowan, Alain Fischer, Andrew R Gennery
BACKGROUND: Rare DNA breakage-repair disorders predispose to infection and lympho-reticular malignancies. Hematopoietic cell transplantation (HCT) is curative but co-administered chemo- or radio-therapy is damaging due to systemic radio-sensitivity. We collected HCT outcome data for Nijmegen Breakage syndrome (NBS), DNA ligase IV deficiency (LIG4), Cernunnos-XLF deficiency and ataxia-telangiectasia. METHODS: Data from 38 centres worldwide, including indication, donor, conditioning regimen, graft-versus-host disease (GvHD) and outcome were analyzed...
April 6, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/28389511/epigenetic-regulation-of-kpc1-ubiquitin-ligase-effects-the-nf-%C3%AE%C2%BAb-pathway-in-melanoma
#3
Yuuki Iida, Aaron Ciechanover, Diego M Marzese, Keisuke Hata, Matias Bustos, Shigeshi Ono, Jinhua Wang, Matthew P Salomon, Kevin Tran, Stella Lam, Sandy C Hsu, Nellie Nelson, Yelena Kravtsova-Ivantsiv, Gordon B Mills, Michael A Davies, Dave Sb Hoon
PURPOSE: Abnormal activation of the NF-κB pathway induces a more aggressive phenotype of cutaneous melanoma. Understanding the mechanisms involved in melanoma NF-κB activation may identify novel targets for this pathway. KPC1, an E3 ubiquitin ligase, is a regulator of NF-κB pathway. The objective of this study was to investigate the mechanisms regulating KPC1 expression and its clinical impact in melanoma. EXPERIMENTAL DESIGN: The clinical impact of KPC1 expression and its epigenetic regulation were assessed in large cohorts of clinically well-annotated melanoma tissues (tissue micro-arrays; n=137, JWCI cohort; n=40) and The Cancer Genome Atlas database (TCGA cohort, n=370)...
April 7, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/28381424/gsk-3-mediated-phosphorylation-couples-er-golgi-transport-and-nuclear-stabilization-of-the-creb-h-transcription-factor-to-mediate-apolipoprotein-secretion
#4
Sónia Barbosa, Suzanne Carreira, Peter O'Hare
CREB-H, an ER-anchored transcription factor, plays a key role in regulating secretion in metabolic pathways, particularly triglyceride homeostasis. It controls the production both of secretory pathway components and cargoes, including apolipoproteins ApoA-IV and ApoC-II, contributing to VLDL/HDL distribution and lipolysis. The key mechanism controlling CREB-H activity involves its ER retention and forward transport to the Golgi, where it is cleaved by Golgi-resident proteases, releasing the N-terminal product, which traffics to the nucleus to effect transcriptional responses...
June 1, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/28361061/non-homologous-end-joining-protein-expression-screen-from-radiosensitive-cancer-patients-yields-a-novel-dna-double-strand-break-repair-phenotype
#5
Michael J McKay, Su Kak Goh, Jeremy N McKay, Michael Chao, Timothy M McKay
BACKGROUND: Clinical radiosensitivity is a significant impediment to tumour control and cure, in that it restricts the total doses which can safely be delivered to the whole radiotherapy population, within the tissue tolerance of potentially radiosensitive (RS) individuals. Understanding its causes could lead to personalization of radiotherapy. METHODS: We screened tissues from a unique bank of RS cancer patients for expression defects in major DNA double-strand break repair proteins, using Western blot analysis and subsequently reverse-transcriptase polymerase chain reaction and pulsed-field gel electrophoresis...
March 2017: Annals of Translational Medicine
https://www.readbyqxmd.com/read/28346336/enzymatic-processes-in-marine-biotechnology
#6
REVIEW
Antonio Trincone
In previous review articles the attention of the biocatalytically oriented scientific community towards the marine environment as a source of biocatalysts focused on the habitat-related properties of marine enzymes. Updates have already appeared in the literature, including marine examples of oxidoreductases, hydrolases, transferases, isomerases, ligases, and lyases ready for food and pharmaceutical applications. Here a new approach for searching the literature and presenting a more refined analysis is adopted with respect to previous surveys, centering the attention on the enzymatic process rather than on a single novel activity...
March 25, 2017: Marine Drugs
https://www.readbyqxmd.com/read/28315454/astragaloside-iv-attenuates-lead-acetate-induced-inhibition-of-neurite-outgrowth-through-activation-of-akt-dependent-nrf2-pathway-in-vitro
#7
Chunlei Yu, Siwen Pan, Miaoxian Dong, Yingcai Niu
Recently, oxidative stress is strongly associated with lead (Pb)-induced neurotoxicity. We reported previously that Astragaloside IV (AS-IV) possesses potent antioxidant properties. Here, we evaluate the hypothesis that AS-IV attenuates lead acetate (PbAc)-mediated inhibition of neurite outgrowth might mainly result from its antioxidant property via serine/threonine protein kinase (Akt)-dependent activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Interestingly, AS-IV attenuates PbAc-induced inhibition of neurite outgrowth and displayed potential antioxidant properties by inhibiting reactive oxygen species (ROS)...
March 14, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28254618/parkin-promotes-proteasomal-degradation-of-synaptotagmin-iv-by-accelerating-polyubiquitination
#8
Hiroyuki Kabayama, Naoko Tokushige, Makoto Takeuchi, Miyuki Kabayama, Mitsunori Fukuda, Katsuhiko Mikoshiba
Parkin is an E3 ubiquitin ligase whose mutations cause autosomal recessive juvenile Parkinson's disease (PD). Unlike the human phenotype, parkin knockout (KO) mice show no apparent dopamine neuron degeneration, although they demonstrate reduced expression and activity of striatal mitochondrial proteins believed to be necessary for neuronal survival. Instead, parkin-KO mice show reduced striatal evoked dopamine release, abnormal synaptic plasticity, and non-motor symptoms, all of which appear to mimic the preclinical features of Parkinson's disease...
February 22, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28133776/non-homologous-end-joining-common-interaction-sites-and-exchange-of-multiple-factors-in-the-dna-repair-process
#9
Stuart L Rulten, Gabrielle J Grundy
Non-homologous end-joining (NHEJ) is the dominant means of repairing chromosomal DNA double strand breaks (DSBs), and is essential in human cells. Fifteen or more proteins can be involved in the detection, signalling, synapsis, end-processing and ligation events required to repair a DSB, and must be assembled in the confined space around the DNA ends. We review here a number of interaction points between the core NHEJ components (Ku70, Ku80, DNA-PKcs, XRCC4 and Ligase IV) and accessory factors such as kinases, phosphatases, polymerases and structural proteins...
March 2017: BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology
https://www.readbyqxmd.com/read/28112597/identification-of-loci-of-pseudomonas-syringae-pv-actinidiae-involved-in-lipolytic-activity-and-their-role-in-colonization-of-kiwifruit-leaves
#10
Hitendra Kumar Patel, Patrizia Ferrante, Meng Xianfa, Sree Gowrinadh Javvadi, Sujatha Subramoni, Marco Scortichini, Vittorio Venturi
Bacterial canker disease caused by Pseudomonas syringae pv. actinidiae, an emerging pathogen of kiwifruit plants, has recently brought about major economic losses worldwide. Genetic studies on virulence functions of P. syringae pv. actinidiae have not yet been reported and there is little experimental data regarding bacterial genes involved in pathogenesis. In this study, we performed a genetic screen in order to identify transposon mutants altered in the lipolytic activity because it is known that mechanisms of regulation, production, and secretion of enzymes often play crucial roles in virulence of plant pathogens...
June 2017: Phytopathology
https://www.readbyqxmd.com/read/28101326/microhomology-mediated-end-joining-new-players-join-the-team
#11
REVIEW
Hailong Wang, Xingzhi Xu
DNA double-strand breaks (DSBs) are the most deleterious type of DNA damage in cells arising from endogenous and exogenous attacks on the genomic DNA. Timely and properly repair of DSBs is important for genomic integrity and survival. MMEJ is an error-prone repair mechanism for DSBs, which relies on exposed microhomologous sequence flanking broken junction to fix DSBs in a Ku- and ligase IV-independent manner. Recently, significant progress has been made in MMEJ mechanism study. In this review, we will summarize its biochemical activities of several newly identified MMEJ factors and their biological significance...
2017: Cell & Bioscience
https://www.readbyqxmd.com/read/28081275/role-of-xrcc1-gene-polymorphisms-in-non-small-cell-lung-cancer-cisplatin-based-chemotherapy-and-their-effect-on-clinical-and-pathological-characteristics
#12
H F Liu, J S Liu, J H Deng, R R Wu
Non-small cell lung cancer (NSCLC) is the most common cancer globally. The XRCC1 protein interacts with ligase and poly(ADP-ribose) polymerase to repair cisplatin-induced DNA damage. The authors of previous studies have reported XRCC1 Arg399Gln, Arg280His, and Arg194Trp polymorphisms and advanced NSCLC prognosis, but the results are inconclusive. We investigated the association between clinical outcome and XRCC1 Arg399Gln, Arg280His, and Arg194Trp polymorphisms in advanced NSCLC patients treated with cisplatin...
December 23, 2016: Genetics and Molecular Research: GMR
https://www.readbyqxmd.com/read/27941919/multiplex-crispr-cas9-based-genome-engineering-enhanced-by-drosha-mediated-sgrna-shrna-structure
#13
Qiang Yan, Kun Xu, Jiani Xing, Tingting Zhang, Xin Wang, Zehui Wei, Chonghua Ren, Zhongtian Liu, Simin Shao, Zhiying Zhang
The clustered regularly interspaced short palindromic repeats (CRISPR) system has recently been developed into a powerful genome-editing technology, as it requires only two key components (Cas9 protein and sgRNA) to function and further enables multiplex genome targeting and homology-directed repair (HDR) based precise genome editing in a wide variety of organisms. Here, we report a novel and interesting strategy by using the Drosha-mediated sgRNA-shRNA structure to direct Cas9 for multiplex genome targeting and precise genome editing...
December 12, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27924007/bridging-of-double-stranded-breaks-by-the-nonhomologous-end-joining-ligation-complex-is-modulated-by-dna-end-chemistry
#14
Dylan A Reid, Michael P Conlin, Yandong Yin, Howard H Chang, Go Watanabe, Michael R Lieber, Dale A Ramsden, Eli Rothenberg
The nonhomologous end-joining (NHEJ) pathway is the primary repair pathway for DNA double strand breaks (DSBs) in humans. Repair is mediated by a core complex of NHEJ factors that includes a ligase (DNA Ligase IV; L4) that relies on juxtaposition of 3΄ hydroxyl and 5΄ phosphate termini of the strand breaks for catalysis. However, chromosome breaks arising from biological sources often have different end chemistries, and how these different end chemistries impact the way in which the core complex directs the necessary transitions from end pairing to ligation is not known...
February 28, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/27915381/regulation-of-non-homologous-end-joining-via-post-translational-modifications-of-components-of-the-ligation-step
#15
REVIEW
Kristína Durdíková, Miroslav Chovanec
DNA double-strand breaks are the most serious type of DNA damage and non-homologous end joining (NHEJ) is an important pathway for their repair. In Saccharomyces cerevisiae, three complexes mediate the canonical NHEJ pathway, Ku (Ku70/Ku80), MRX (Mre11/Rad50/Xrs2) and DNA ligase IV (Dnl4/Lif1). Mammalian NHEJ is more complex, primarily as a consequence of the fact that more factors are involved in the process, and also because higher chromatin organization and more complex regulatory networks exist in mammals...
December 3, 2016: Current Genetics
https://www.readbyqxmd.com/read/27875301/an-intrinsically-disordered-aplf-links-ku-dna-pkcs-and-xrcc4-dna-ligase-iv-in-an-extended-flexible-non-homologous-end-joining-complex
#16
Michal Hammel, Yaping Yu, Sarvan K Radhakrishnan, Chirayu Chokshi, Miaw-Sheue Tsai, Yoshihiro Matsumoto, Monica Kuzdovich, Soumya G Remesh, Shujuan Fang, Alan E Tomkinson, Susan P Lees-Miller, John A Tainer
DNA double-strand break (DSB) repair by non-homologous end joining (NHEJ) in human cells is initiated by Ku heterodimer binding to a DSB, followed by recruitment of core NHEJ factors including DNA-dependent protein kinase catalytic subunit (DNA-PKcs), XRCC4-like factor (XLF), and XRCC4 (X4)-DNA ligase IV (L4). Ku also interacts with accessory factors such as aprataxin and polynucleotide kinase/phosphatase-like factor (APLF). Yet, how these factors interact to tether, process, and ligate DSB ends while allowing regulation and chromatin interactions remains enigmatic...
December 30, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27872982/interplay-between-top1-and-mms21-nse2-mediated-sumoylation-in-stable-maintenance-of-long-chromosomes
#17
Lakshmi Mahendrawada, Ragini Rai, Deepash Kothiwal, Shikha Laloraya
Genetic information in cells is encrypted in DNA molecules forming chromosomes of varying sizes. Accurate replication and partitioning of chromosomes in the crowded cellular milieu is a complex process involving duplication, folding and movement. Longer chromosomes may be more susceptible to mis-segregation or DNA damage and there may exist specialized physiological mechanisms preventing this. Here, we present genetic evidence for such a mechanism which depends on Mms21/Nse2 mediated sumoylation and topoisomerase-1 (Top1) for maintaining stability of longer chromosomes...
November 21, 2016: Current Genetics
https://www.readbyqxmd.com/read/27855655/two-hits-in-one-whole-genome-sequencing-unveils-lig4-syndrome-and-urofacial-syndrome-in-a-case-report-of-a-child-with-complex-phenotype
#18
Abeer Fadda, Fiza Butt, Sara Tomei, Sara Deola, Bernice Lo, Amal Robay, Alya Al-Shakaki, Noor Al-Hajri, Ronald Crystal, Marios Kambouris, Ena Wang, Francesco M Marincola, Khalid A Fakhro, Chiara Cugno
BACKGROUND: Ligase IV syndrome, a hereditary disease associated with compromised DNA damage response mechanisms, and Urofacial syndrome, caused by an impairment of neural cell signaling, are both rare genetic disorders, whose reports in literature are limited. We describe the first case combining both disorders in a specific phenotype. CASE PRESENTATION: We report a case of a 7-year old girl presenting with a complex phenotype characterized by multiple congenital abnormalities and dysmorphic features, microcephaly, short stature, combined immunodeficiency and severe vesicoureteral reflux...
November 17, 2016: BMC Medical Genetics
https://www.readbyqxmd.com/read/27853172/lithium-promotes-dna-stability-and-survival-of-ischemic-retinal-neurocytes-by-upregulating-dna-ligase-iv
#19
Ying Yang, Nandan Wu, Sijia Tian, Fan Li, Huan Hu, Pei Chen, Xiaoxiao Cai, Lijun Xu, Jing Zhang, Zhao Chen, Jian Ge, Keming Yu, Jing Zhuang
Neurons display genomic fragility and show fragmented DNA in pathological degeneration. A failure to repair DNA breaks may result in cell death or apoptosis. Lithium protects retinal neurocytes following nutrient deprivation or partial nerve crush, but the underlying mechanisms are not well defined. Here we demonstrate that pretreatment with lithium protects retinal neurocytes from ischemia-induced damage and enhances light response in rat retina following ischemia-reperfusion injury. Moreover, we found that DNA nonhomologous end-joining (NHEJ) repair is implicated in this process because in ischemic retinal neurocytes, lithium significantly reduces the number of γ-H2AX foci (well-characterized markers of DNA double-strand breaks in situ) and increases the DNA ligase IV expression level...
November 17, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27852949/transcriptional-gene-silencing-maintained-by-ots1-sumo-protease-requires-a-dna-dependent-polymerase-v-dependent-pathway
#20
Lei Liu, Xiaojing Yan, Xiangxiong Kong, Yiqiang Zhao, Zhizhong Gong, Jing Bo Jin, Yan Guo
The expression of genes with aberrant structure is prevented at both the transcriptional and posttranscriptional regulation levels. Aberrant gene silencing at the posttranscriptional level is well studied; however, it is not well understood how aberrant genes are silenced at the transcriptional level. In this study, through genetic screening a transgenic report line that harbors an aberrant gene (35S-LUC, lacking 3'-untranslated region [3'-UTR]) and lacks luciferase (LUC) activity, we identify that the small ubiquitin-like modifier (SUMO) protease OTS1 gene is required for maintaining the silence of the reporter 35S-LUC and an endogenous mutator-like element MULE-F19G14 at the transcriptional level, which requires DNA-dependent RNA polymerase (Pol) V and DDR complex, but not Pol IV...
January 2017: Plant Physiology
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