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Monoubiquitination

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https://www.readbyqxmd.com/read/29130659/-dna-repair-function-and-mutation-of-an-h2b-monoubiquitination-factor-wdr70-in-ovarian-cancer
#1
Zi-Zhi Tang, Hai-Bin Wang, Ming Zeng, Cong Liu, De-Hua Li
OBJECTIVE: To investigate the roles of enzyme DCAF proteinDNA damagebinding protein 1 (DDB1)/cullin4 (CRL4) complex family members CRL4WD40 repeat domain protein 70 (WDR70) in DNA repair process and its mutation in ovarian cancer. METHODS: Immunofluorescent assay was employed to measure H2AX (γH2AX) and phosphorylated replication protein A2 (RPA32) formed in siDDB1 or siWDR70 ovarian cancer cells after the treatments of chemical medicine and radioactive threapy...
September 2017: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
https://www.readbyqxmd.com/read/29111344/the-crystal-structure-and-conformations-of-an-unbranched-mixed-tri-ubiquitin-chain-containing-k48-and-k63-linkages
#2
Prasanth Padala, Nadine Soudah, Moshe Giladi, Yoni Haitin, Michail N Isupov, Reuven Wiener
The ability of ubiquitin to function in a wide range of cellular processes is ascribed to its capacity to cause a diverse spectrum of modifications. While a target protein can be modified with monoubiquitin, it can also be modified with ubiquitin chains. The latter include seven types of homotypic chains as well as mixed ubiquitin chains. In a mixed chain, not all the isopeptide bonds are restricted to a specific lysine of ubiquitin, resulting in a chain possessing more than one type of linkage. While structural characterization of homotypic chains has been well elucidated, less is known about mixed chains...
October 27, 2017: Journal of Molecular Biology
https://www.readbyqxmd.com/read/29100324/modulation-of-the-fanconi-anemia-pathway-via-chemically-induced-changes-in-chromatin-structure
#3
David A Vierra, Jada L Garzon, Meghan A Rego, Morganne M Adroved, Maurizio Mauro, Niall G Howlett
Fanconi anemia (FA) is a rare disease characterized by congenital defects, bone marrow failure, and atypically early-onset cancers. The FA proteins function cooperatively to repair DNA interstrand crosslinks. A major step in the activation of the pathway is the monoubiquitination of the FANCD2 and FANCI proteins, and their recruitment to chromatin-associated nuclear foci. The regulation and function of FANCD2 and FANCI, however, is poorly understood. In addition, how chromatin state impacts pathway activation is also unknown...
September 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/29093085/the-ubiquitin-proteasome-system-is-necessary-for-the-efficient-replication-of-human-astrovirus
#4
Luis A Casorla-Pérez, Tomás López, Susana López, Carlos F Arias
Astroviruses, members of the family Astroviridae, represent an important cause of human gastroenteritis in the world. The cellular factors required for astrovirus replication have been poorly studied. In this work, we evaluated the relevance of the ubiquitin-proteasome system (UPS) in the replication of Yuc8, a human astrovirus serotype 8 strain. We found that proteasome inhibitors decrease the production of infectious viral progeny at a step in the replication cycle subsequent to virus entry. The inhibition of the proteasome activity decreases viral RNA levels and viral protein synthesis; similarly, the inhibition of ubiquitination by chemical inhibitors or RNAi reduces the production of viral progeny as well as viral protein synthesis...
November 1, 2017: Journal of Virology
https://www.readbyqxmd.com/read/29059323/fanci-and-fancd2-have-common-as-well-as-independent-functions-during-the-cellular-replication-stress-response
#5
Elizabeth L Thompson, Jung E Yeo, Eun-A Lee, Yinan Kan, Maya Raghunandan, Constanze Wiek, Helmut Hanenberg, Orlando D Schärer, Eric A Hendrickson, Alexandra Sobeck
Fanconi anemia (FA) is an inherited cancer predisposition syndrome characterized by cellular hypersensitivity to DNA interstrand crosslinks (ICLs). To repair these lesions, the FA proteins act in a linear hierarchy: following ICL detection on chromatin, the FA core complex monoubiquitinates and recruits the central FANCI and FANCD2 proteins that subsequently coordinate ICL removal and repair of the ensuing DNA double-stranded break by homology-dependent repair (HDR). FANCD2 also functions during the replication stress response by mediating the restart of temporarily stalled replication forks thereby suppressing the firing of new replication origins...
November 16, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/29058668/e3-ubiquitin-ligase-bre1-couples-sister-chromatid-cohesion-establishment-to-dna-replication-in-saccharomyces-cerevisiae
#6
Wei Zhang, Clarence Hue Lok Yeung, Liwen Wu, Karen Wing Yee Yuen
Bre1, a conserved E3 ubiquitin ligase in Saccharomyces cerevisiae, together with its interacting partner Lge1, are responsible for histone H2B monoubiquitination, which regulates transcription, DNA replication, DNA damage response and repair, ensuring the structural integrity of the genome. Deletion of BRE1 or LGE1 also results in whole chromosome instability. We discovered a novel role for Bre1, Lge1 and H2Bub1 in chromosome segregation and sister chromatid cohesion. Bre1's function in G1 and S phases contributes to cohesion establishment, but it is not required for cohesion maintenance in G2 phase...
October 23, 2017: ELife
https://www.readbyqxmd.com/read/29048607/the-arabidopsis-chromatin-remodeling-factor-chr5-regulates-plant-immune-responses-and-nucleosome-occupancy
#7
Baohong Zou, Qi Sun, Wenli Zhang, Yuan Ding, Dong-Lei Yang, Jian Hua
ATP-dependent chromatin remodeling factors use the energy of ATP hydrolysis to alter the structure of chromatin and are important regulators of eukaryotic gene expression. One such factor CHR5 (Chromatin Remodeling Factor 5) in Arabidopsis (Arabidopsis thaliana) was previously found to be involved in growth and development regulation. Here we show that CHR5 is required for the upregulation of the intracellular immune receptor gene SNC1 (SUPPRESSOR OF npr1-1, CONSTITUTIVE1) and consequently the autoimmunity induced by SNC1 upregulation...
October 17, 2017: Plant & Cell Physiology
https://www.readbyqxmd.com/read/29021208/constitutive-role-of-the-fanconi-anemia-d2-gene-in-the-replication-stress-response
#8
Yanyan Tian, Xi Shen, Rui Wang, Naeh Klages-Mundt, Erica J Lynn, Sara K Martin, Yin Ye, Min Gao, Junjie Chen, Katharina Schlacher, Lei Li
In response to DNA crosslinking damage, the Fanconi anemia (FA) core complex activates the FA pathway by monoubiquitinating Fanconi anemia complementation group D2 (FANCD2) for the initiation of the nucleolytic processing of the DNA crosslinks and stabilization of stalled replication forks. Given that all the classic FA proteins coordinately monoubiquitinate FANCD2, it is unclear why losses of individual classic FA genes yield varying cellular sensitivities to crosslinking damage. To address this question, we generated cellular knockout models of FA core complex components and FANCD2 and found that FANCD2-null mutants display higher levels of spontaneous chromosomal damage and hypersensitivity to replication-blocking lesions than Fanconi anemia complementation group L (FANCL)-null mutants, suggesting that FANCD2 provides a basal level of DNA protection countering endogenous lesions in the absence of monoubiquitination...
October 11, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28968219/site-specific-monoubiquitination-downregulates-rab5-by-disrupting-effector-binding-and-guanine-nucleotide-conversion
#9
Donghyuk Shin, Wooju Na, Ji-Hyung Lee, Gyuhee Kim, Jiseok Baek, Seok Hee Park, Cheol Yong Choi, Sangho Lee
Rab GTPases, which are involved in intracellular trafficking pathways, have recently been reported to be ubiquitinated. However, the functions of ubiquitinated Rab proteins remain unexplored. Here we show that Rab5 is monoubiquitinated on K116, K140, and K165. Upon co-transfection with ubiquitin, Rab5 exhibited abnormalities in endosomal localization and EGF-induced EGF receptor degradation. Rab5 K140R and K165R mutants restored these abnormalities, whereas K116R did not. We derived structural models of individual monoubiquitinated Rab5 proteins (mUbRab5s) by solution scattering and observed different conformational flexibilities in a site-specific manner...
October 2, 2017: ELife
https://www.readbyqxmd.com/read/28947091/the-ubiquitin-code-in-the-ubiquitin-proteasome-system-and-autophagy
#10
REVIEW
Yong Tae Kwon, Aaron Ciechanover
The conjugation of the 76 amino acid protein ubiquitin to other proteins can alter the metabolic stability or non-proteolytic functions of the substrate. Once attached to a substrate (monoubiquitination), ubiquitin can itself be ubiquitinated on any of its seven lysine (Lys) residues or its N-terminal methionine (Met1). A single ubiquitin polymer may contain mixed linkages and/or two or more branches. In addition, ubiquitin can be conjugated with ubiquitin-like modifiers such as SUMO or small molecules such as phosphate...
November 2017: Trends in Biochemical Sciences
https://www.readbyqxmd.com/read/28946194/esculetin-ameliorates-vascular-perturbation-by-intervening-in-the-occupancy-of-h2bk120ub-at-at1-at2-tgf%C3%AE-1-and-mcp1-promoter-gene-in-thoracic-aorta-of-ir-and-t2d-rats
#11
Almesh Kadakol, Santosh Kumar Goru, Vajir Malek, Anil Bhanudas Gaikwad
Micro and macro vascular complications under diabetic condition are the responses to pathological stimuli exerted by up regulated renin angiotensin system (RAS) via deteriorating vascular physiology. Up-regulated RAS could influence in the adaptive mechanisms of target tissues to alter the abundance of angiotensin II type 1 receptor (AT1) and angiotensin II type 2 receptor (AT2). Such differential regulation of AT1 and AT2 have been reported to be associated with post-translational histone modifications (PTHMs)...
November 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28945249/mechanism-and-regulation-of-the-lys6-selective-deubiquitinase-usp30
#12
Malte Gersch, Christina Gladkova, Alexander F Schubert, Martin A Michel, Sarah Maslen, David Komander
Damaged mitochondria undergo mitophagy, a specialized form of autophagy that is initiated by the protein kinase PINK1 and the ubiquitin E3 ligase Parkin. Ubiquitin-specific protease USP30 antagonizes Parkin-mediated ubiquitination events on mitochondria and is a key negative regulator of mitophagy. Parkin and USP30 both show a preference for assembly or disassembly, respectively, of Lys6-linked polyubiquitin, a chain type that has not been well studied. Here we report crystal structures of human USP30 bound to monoubiquitin and Lys6-linked diubiquitin, which explain how USP30 achieves Lys6-linkage preference through unique ubiquitin binding interfaces...
November 2017: Nature Structural & Molecular Biology
https://www.readbyqxmd.com/read/28925810/ube3a-mediated-regulation-of-imprinted-genes-and-epigenome-wide-marks-in-human-neurons
#13
S Jesse Lopez, Keith Dunaway, M Saharul Islam, Charles Mordaunt, Annie Vogel Ciernia, Makiko Meguro-Horike, Shin-Ichi Horike, David J Segal, Janine LaSalle
The dysregulation of genes in neurodevelopmental disorders that lead to social and cognitive phenotypes is a complex, multilayered process involving both genetics and epigenetics. Parent-of-origin effects of deletion and duplication of the 15q11-q13 locus leading to Angelman, Prader-Willi, and Dup15q syndromes are due to imprinted genes, including UBE3A, which is maternally expressed exclusively in neurons. UBE3A encodes a ubiquitin E3 ligase protein with multiple downstream targets, including RING1B, which in turn monoubiquitinates histone variant H2A...
September 19, 2017: Epigenetics: Official Journal of the DNA Methylation Society
https://www.readbyqxmd.com/read/28918480/sgs1-helicase-is-required-for-efficient-pcna-monoubiquitination-and-translesion-dna-synthesis-in-saccharomyces-cerevisiae
#14
Fangfang Li, Lindsay G Ball, Li Fan, Michelle Hanna, Wei Xiao
DNA-damage tolerance (DDT) is employed by eukaryotes to deal with replication blocks on the template strand, and is divided into two parallel pathways that are activated by sequential ubiquitination of proliferating cell nuclear antigen (PCNA) at the Lys164 residue. Rad6-Rad18-mediated PCNA monoubiquitination promotes translesion DNA synthesis (TLS) and the monoubiquitinated PCNA can be further polyubiquitinated by an Mms2-Ubc13-Rad5 complex, leading to error-free lesion bypass. We previously reported that the DNA helicase Sgs1 is required for error-free lesion bypass, probably through the double-Holliday junction migration and subsequent resolution...
September 16, 2017: Current Genetics
https://www.readbyqxmd.com/read/28886337/replication-fork-slowing-and-reversal-upon-dna-damage-require-pcna-polyubiquitination-and-zranb3-dna-translocase-activity
#15
Marko Vujanovic, Jana Krietsch, Maria Chiara Raso, Nastassja Terraneo, Ralph Zellweger, Jonas A Schmid, Angelo Taglialatela, Jen-Wei Huang, Cory L Holland, Katharina Zwicky, Raquel Herrador, Heinz Jacobs, David Cortez, Alberto Ciccia, Lorenza Penengo, Massimo Lopes
DNA damage tolerance during eukaryotic replication is orchestrated by PCNA ubiquitination. While monoubiquitination activates mutagenic translesion synthesis, polyubiquitination activates an error-free pathway, elusive in mammals, enabling damage bypass by template switching. Fork reversal is driven in vitro by multiple enzymes, including the DNA translocase ZRANB3, shown to bind polyubiquitinated PCNA. However, whether this interaction promotes fork remodeling and template switching in vivo was unknown. Here we show that damage-induced fork reversal in mammalian cells requires PCNA ubiquitination, UBC13, and K63-linked polyubiquitin chains, previously involved in error-free damage tolerance...
September 7, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28865289/dna-polymerase-%C3%AE-the-long-and-the-short-of-it
#16
Ekaterina G Frank, Mary P McLenigan, John P McDonald, Donald Huston, Samantha Mead, Roger Woodgate
The cDNA encoding human DNA polymerase ι (POLI) was cloned in 1999. At that time, it was believed that the POLI gene encoded a protein of 715 amino acids. Advances in DNA sequencing technologies led to the realization that there is an upstream, in-frame initiation codon that would encode a DNA polymerase ι (polι) protein of 740 amino acids. The extra 25 amino acid region is rich in acidic residues (11/25) and is reasonably conserved in eukaryotes ranging from fish to humans. As a consequence, the curated Reference Sequence (RefSeq) database identified polι as a 740 amino acid protein...
October 2017: DNA Repair
https://www.readbyqxmd.com/read/28859169/the-replication-initiator-protein-of-a-geminivirus-interacts-with-host-monoubiquitination-machinery-and-stimulates-transcription-of-the-viral-genome
#17
Nirbhay Kumar Kushwaha, Mansi Bhardwaj, Supriya Chakraborty
Geminiviruses constitute a group of plant viruses, with a ssDNA genome, whose replication in the nucleus of an infected cell requires the function of geminivirus-encoded replication initiator protein (Rep). Our results suggest that monoubiquitinated histone 2B (H2B-ub) promotes tri-methylation of histone 3 at lysine 4 (H3-K4me3) on the promoter of Chilli leaf curl virus (ChiLCV). We isolated homologues of two major components of the monoubiquitination machinery: UBIQUITIN-CONJUGATING ENZYME2 (NbUBC2) and HISTONE MONOUBIQUITINATION1 (NbHUB1) from N...
August 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28855448/caffeine-has-a-synergistic-anticancer-effect-with-cisplatin-via-inhibiting-fanconi-anemia-group-d2-protein-monoubiquitination-in-hepatocellular-carcinoma-cells
#18
Yuichiro Oda, Muneaki Hidaka, Akito Suzuki
Cisplatin is an anticancer agent and induces DNA interstrand cross-links (ICLs). ICLs activate various signaling processes and induce DNA repair pathways, including the Fanconi anemia (FA) pathway. FA complementation group D2 (FANCD2) is monoubiquitinated in response to DNA damage, leading to activation of the DNA double-strand-break repair protein, RAD51. Caffeine increases the anticancer activity of cisplatin by inhibiting DNA repair; however, details of the mechanism remain unclear. We investigated the mechanism responsible for the synergistic anticancer effect of cisplatin and caffeine in HepG2 human hepatocellular carcinoma cells, focusing on the FA pathway...
August 31, 2017: Biological & Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/28841006/esi-im-ms-and-collision-induced-unfolding-that-provide-insight-into-the-linkage-dependent-interfacial-interactions-of-covalently-linked-diubiquitin
#19
Nicole D Wagner, David E Clemmer, David H Russell
Understanding protein higher order structure and interfacial interactions is crucial to understanding protein binding motifs and cellular function, that is, an interactome. Polyubiquitylation is a post-translational modification that functions as a tag for a diverse array of cellular processes, wherein differences in chain length, branching, and linkage site encode different cellular functions. Investigation of covalently linked diubiquitin (diUbq) molecules specifically selects for the effect of covalent linkage site on the conformational preference of the molecule and the interfacial interactions between the subunits...
August 31, 2017: Analytical Chemistry
https://www.readbyqxmd.com/read/28837157/biallelic-truncating-fancm-mutations-cause-early-onset-cancer-but-not-fanconi-anemia
#20
Massimo Bogliolo, Dominique Bluteau, James Lespinasse, Roser Pujol, Nadia Vasquez, Catherine Dubois d'Enghien, Dominique Stoppa-Lyonnet, Thierry Leblanc, Jean Soulier, Jordi Surrallés
PurposeMutations in genes involved in Fanconi anemia (FA)/BRCA DNA repair pathway cause cancer susceptibility diseases including familial breast cancer and Fanconi anemia (FA). A single FA patient with biallelic FANCM mutations was reported in 2005 but concurrent FANCA pathogenic mutations precluded assignment of FANCM as an FA gene. Here we report three individuals with biallelic FANCM truncating mutations who developed early-onset cancer and toxicity to chemotherapy but did not present congenital malformations or any hematological phenotype suggestive of FA...
August 24, 2017: Genetics in Medicine: Official Journal of the American College of Medical Genetics
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