Littérature scientifique sur le sujet « RNF216 »
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Articles de revues sur le sujet "RNF216"
Melnick, Ashley F., Yuen Gao, Jiali Liu, Deqiang Ding, Alicia Predom, Catherine Kelly, Rex A. Hess et Chen Chen. « RNF216 is essential for spermatogenesis and male fertility† ». Biology of Reproduction 100, no 5 (15 janvier 2019) : 1132–34. http://dx.doi.org/10.1093/biolre/ioz006.
Texte intégralSeenivasan, Ramkumar, Thomas Hermanns, Tamara Blyszcz, Michael Lammers, Gerrit J. K. Praefcke et Kay Hofmann. « Mechanism and chain specificity of RNF216/TRIAD3, the ubiquitin ligase mutated in Gordon Holmes syndrome ». Human Molecular Genetics 28, no 17 (24 avril 2019) : 2862–73. http://dx.doi.org/10.1093/hmg/ddz098.
Texte intégralGanos, Christos, Joshua Hersheson, Matthew Adams, Kailash P. Bhatia et Henry Houlden. « Syndromic associations and RNF216 mutations ». Parkinsonism & ; Related Disorders 21, no 11 (novembre 2015) : 1389–90. http://dx.doi.org/10.1016/j.parkreldis.2015.09.010.
Texte intégralGanos, Christos, Joshua Hersheson, Matthew Adams, Kailash P. Bhatia et Henry Houlden. « The 4H syndrome due to RNF216 mutation ». Parkinsonism & ; Related Disorders 21, no 9 (septembre 2015) : 1122–23. http://dx.doi.org/10.1016/j.parkreldis.2015.07.012.
Texte intégralWolf, Nicole I., et Geneviève Bernard. « Mutations in RNF216 do not cause 4H syndrome ». Parkinsonism & ; Related Disorders 21, no 11 (novembre 2015) : 1387–88. http://dx.doi.org/10.1016/j.parkreldis.2015.09.014.
Texte intégralXu, Congfeng, Kuan Feng, Xiaonan Zhao, Shiqian Huang, Yiji Cheng, Liu Qian, Yanan Wang et al. « Regulation of autophagy by E3 ubiquitin ligase RNF216 through BECN1 ubiquitination ». Autophagy 10, no 12 (11 novembre 2014) : 2239–50. http://dx.doi.org/10.4161/15548627.2014.981792.
Texte intégralSantens, P., T. Van Damme, W. Steyaert, A. Willaert, B. Sablonniere, A. De Paepe, P. J. Coucke et B. Dermaut. « RNF216 mutations as a novel cause of autosomal recessive Huntington-like disorder ». Neurology 84, no 17 (3 avril 2015) : 1760–66. http://dx.doi.org/10.1212/wnl.0000000000001521.
Texte intégralCalandra, Cristian R., Yamile Mocarbel, Sebastian A. Vishnopolska, Vanessa Toneguzzo, Jaen Oliveri, Enrique Carlos Cazado, German Biagioli, Adrián G. Turjanksi et Marcelo Marti. « Gordon Holmes Syndrome Caused by RNF216 Novel Mutation in 2 Argentinean Siblings ». Movement Disorders Clinical Practice 6, no 3 (16 janvier 2019) : 259–62. http://dx.doi.org/10.1002/mdc3.12721.
Texte intégralChen, Ke‐Liang, Gui‐Xian Zhao, He Wang, Lei Wei, Yu‐Yuan Huang, Shi‐Dong Chen, Bi‐Ying Lin, Qiang Dong, Mei Cui et Jin‐Tai Yu. « A novel de novo RNF216 mutation associated with autosomal recessive Huntington‐like disorder ». Annals of Clinical and Translational Neurology 7, no 5 (mai 2020) : 860–64. http://dx.doi.org/10.1002/acn3.51047.
Texte intégralYoung, J., I. Abdennebi, F. Magnin, L. Maione, J. Bouligand et I. Beau. « Mutations bialléliques de RNF216 dans l’hypogonadisme hypogonadotrophique avec ataxie cérébelleuse : conséquences fonctionnelles sur l’autophagie ». Annales d'Endocrinologie 83, no 5 (octobre 2022) : 317. http://dx.doi.org/10.1016/j.ando.2022.07.108.
Texte intégralThèses sur le sujet "RNF216"
Roewenstrunk, Julia Maria 1981. « RNF169 and RNF168 novel substrates of DYRK1A : connecting DYRK1A to DNA-damage repair ». Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/565442.
Texte intégralAlteraciones de la dosis génica de la quinasa DYRK1A son causantes de enfermedad en humanos. Para profundizar en las actividades biológicas de DYRK1A, se ha realizado un estudio de interactoma, en el que RNF169, elemento clave en la respuesta al daño al DNA causado por roturas de doble cadena, se reveló como uno de los principales interactores. La interacción DYRK1A-RNF169 es directa y responsable de la localización de DYRK1A en el DNA en respuesta al daño. La combinación de espectrometría de masas, mutagénesis y ensayos quinasa ha permitido identificar varios residuos fosforilados por DYRK1A en RNF169 y en su parálogo RNF168, que actúa en el mismo proceso. El silenciamiento de DYRK1A causa alteraciones en los mecanismos de respuesta al daño y las células presentan un aumento de la sensibilidad a la radiación. Estos resultados permiten sugerir que DYRK1A puede ser un nuevo regulador de la respuesta al daño al DNA.
Ng, Jia Nian, et 黃嘉年. « RNF168 expression in breast cancer ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206551.
Texte intégralpublished_or_final_version
Pathology
Master
Master of Medical Sciences
Morimoto, Takaaki. « Significant association of RNF213 p.R4810K, a moyamoya susceptibility variant, with coronary artery disease ». Kyoto University, 2019. http://hdl.handle.net/2433/242398.
Texte intégralROCCHIO, FRANCESCA. « Insights into the RNF168-dependent ubiquitin signalling ». Doctoral thesis, Università del Piemonte Orientale, 2016. http://hdl.handle.net/11579/115175.
Texte intégralTakeda, Midori. « Moyamoya disease patient mutations in the RING domain of RNF213 reduce its ubiquitin ligase activity and enhance NFκB activation and apoptosis in an AAA+ domain-dependent manner ». Kyoto University, 2020. http://hdl.handle.net/2433/259017.
Texte intégralKe, Qi. « Negative Regulation of Host Innate Immune Signaling and Response Pathways by Viral and Host Regulatory Factors ». University of Toledo / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1470185159.
Texte intégralRoy, Vincent. « Modélisation de maladies cérébrovasculaires associées aux variations génétiques de RNF213 par le génie tissulaire et la culture cellulaire 3D ». Doctoral thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/67126.
Texte intégralRNF213 has been associated as a susceptibility gene for the development cerebrovascular diseases (CVDs), in particular, moyamoya disease (MMD) and intracranial aneurysms (ICA). While the exact biological functions of RNF213 remain to be demonstrated, it is known to be involved in the regulation of cell proliferation, angiogenesis and inflammation. The work presented in this thesis focuses on the development of vascular models in vitro to better characterize the role of RNF213 in CVDs. The hypothesis is that the complete invalidation of the RNF213 protein in brain endothelial cells (EC) could recreate evident phenotypes associated with the development of MMD and the formation of ICA. We have initially generated human brain microvascular endothelial cells (hCMEC/D3) deficient in RNF213 (RNF213-/- ) using the robust CRISPR-Cas9 double nickase method. At first, our work described the role that RNF213 would play in the homeostasis of the blood-brain barrier (BBB) maintenance and in the early stages of MMD pathogenesis. More specifically, the loss of adherent junctions caused by the invalidation of RNF213 in hCMEC/D3 was evaluated in vitro on several parameters, such as endothelial morphology, gene expression of junctional proteins, cellular localization, permeability, immune infiltration and the secretome of inflammatory cytokines. Our data demonstrated that RNF213 deficiency provokes a significant decrease in the platelet endothelial cell adhesion molecule-1 (PECAM-1) expression, which consequently affects the proper formation of the junctional complex. A decrease in the expression of the claudin-5, b-catenin and plakoglobin genes was also measured. In addition, RNF213 loss is accompanied with a release of several pro-inflammatory cytokines. Thereafter, the present work also demonstrated that RNF213 plays a preponderant role in the angiogenic process of hCMEC/D3. Angiogenesis has also been characterized on several aspects, such as proliferation, migration, formation of micro-capillaries on a Matrigel®-based support and in a 3D model reconstructed by tissue engineering, gene expression and secretion of angiogenic factors. Our data demonstrates a decrease in cell division rate and an increase in cell migration. In vitro studies have also shown, for the first time, a significant increase in micro-capillary formation and abundant secretion of pro-angiogenic factors, such as the vascular endothelial growth factor (VEGF). More precisely, the hCMEC/D3 deficient in RNF213 forms a wider, denser and more extensive network of micro-capillaries on a Matrigel®-based support. When seeded in a more structurally complex 3D model, hCMEC/D3 form a network that can resemble to the compensatory capillary network found in MMM patients. Overall, the invalidation of the RNF213 gene in a 3D in vitro model of cerebral endothelial cells makes it possible to reproduce certain pathological phenotypes of MMM and v therefore becomes the 1st in vitro model for the study of this disease and other diseases associated with RNF213. Finally, we developed a new model of small-caliber blood vessels reconstructed by tissue engineering (TEBV) to be used to study vascular diseases and complex CVD in vitro. The direct seeding of fibroblasts or smooth muscle cells (CML) onto a polyethylene terephthalate glycol (PETG) mandrel that was pretreated with ultraviolet C (UV-C) radiation facilitate the formation of circular cell sheets, which could be manipulated and stacked in top of each other. Using this novel technique, we were able to successfully generate complete TEBVs with the three main arterial layers: the adventitia, the media and the intima tunica. Taken together, our TEBV model has histological and mechanical properties similar to native human arteries. Furthermore, this optimized and standardized 3D vascular construct will accelerate the scientific progress to modelized complex vascular pathologies, such as MMD and AIC. Indeed, the generation of complete vessels derived from pathological cells or genetically edited cells could facilitate the characterization of pathogenesis and help in the development of drugs.
Arimoto, Keiichiro. « Negative regulation of the RIG-I signaling by the ubiquitin ligase RNF125 ». Kyoto University, 2009. http://hdl.handle.net/2433/124282.
Texte intégralKrysztofinska, Ewelina Maria. « The roles of the co-chaperone SGTA/Sgt2, the BAG6 complex and E3 ubiquitin ligase RNF126 in cytosolic quality control ». Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/the-roles-of-the-cochaperone-sgtasgt2-the-bag6-complex-and-e3-ubiquitin-ligase-rnf126-in-cytosolic-quality-control(9ebe2932-8331-454f-9291-f75ab6619c02).html.
Texte intégralAlemany, Schmidt Alexandra. « Bases moleculares de la meiosis en mamíferos ». Doctoral thesis, Universitat de les Illes Balears, 2017. http://hdl.handle.net/10803/458994.
Texte intégral- Introducción: La meiosis es un tipo de división celular íntimamente ligado a la gametogénesis en eucariotas superiores, la finalidad es la reducción del número cromosómico de diploide a haploide (es decir, de 2n a n) en el núcleo de los gametos. En la presente tesis se han analizado los procesos de sinapsis y recombinación en tres especies de mamíferos: humanos, gatos y perros. - Contenido de la investigación: Para el análisis de los procesos de sinapsis y recombinación en tres especies de mamíferos (humanos, gatos y perros) se ha utilizado la técnica de inmunocitogenética, la cual ha permitido determinar los valores cuantitativos y las características cualitativas de estos procesos. - Conclusión: La infertilidad atribuible a alteraciones en procesos de recombinación y sinapsis cromosómica en autosomas y cuerpo sexual se restringe a aquellos individuos que presentan desviaciones extremas respecto del rango control de estos parámetros. Existe un fenotipo meiótico recurrente, caracterizado por bloqueo en la transición zigoteno-paquiteno. La aplicación de técnicas de NGS (análisis del exoma) en este individuo infértil ha permitido localizar una mutación en el gen TEX11, probablemente patogénica y responsable de las características asociadas a este fenotipo. El análisis de la relación de las variantes alélicas del gen PRDM9 con problemas de fertilidad y generación de síndromes de novo no detectó una asociación significativa en ningún caso. La influencia del gen RNF212 sobre la variabilidad interindividual de la recombinación observada en el presente estudio está asociada a la presencia de polimorfismos genéticos en ese gen. Así, cada copia del alelo T en el SNP rs3796619 de este gen supone una disminución media de la tasa de recombinación de 132,5 cM en comparación con el alelo C. Existe una relación compleja entre los genotipos de PRDM9 y la tasa de recombinación, que parece estar determinada por la longitud de los alelos, por el estado de homozigosidad o heterozigosidad de los mismos y por efectos de dominancia. Hay una gran variabilidad intraindividual de los aspectos cuantitativos y cualitativos de la recombinación y sinapsis en las tres especies analizadas. Esta variabilidad sugiere que, en mamíferos, estos procesos y los factores que los controlan deben ser lo suficientemente flexibles para permitir generar diversidad, aunque dentro de unos márgenes que garanticen la estabilidad genómica. Se han observado diferencias notables en los procesos de recombinación entre humanos y gatos. Así, en gatos se ha determinado la ausencia de picos de recombinación en las regiones subteloméricas, un menor efecto inhibidor del centrómero y una distribución más uniforme a lo largo de los brazos cromosómicos. Estas dos últimas observaciones están relacionadas con la menor interferencia observada en esta especie. Se han observado características sinápticas propias de gatos macho, no descritas hasta el momento, como la presencia de un reservorio de proteína SYCP3 desde leptoteno hasta paquiteno inicial, la separación prematura de los elementos laterales a partir del paquiteno tardío o la morfología propia y cambiante del cuerpo sexual que, al igual que en humanos, puede asociarse al subestadio de esta fase meiótica. Se han detectado anomalías sinápticas en humanos, gatos y perros, aunque la incidencia de asinapsis, gaps y MSUC varió entre especies. Además, se ha descrito por primera vez en estas tres especies el fenómeno de MSUC en individuos sin alteraciones cromosómicas de poblaciones salvajes. En el cuerpo sexual, se ha detectado presencia de proteína SYCP1 más allá de la región PAR en las tres especies analizadas. Esta presencia podría relacionarse con un proceso de polimerización por defecto de la proteína SYCP1, que ayudaría a la reparación de los DSBs situados en el cromosoma X.
- Introduction: Meiosis is a type of cell division intimately linked to gametogenesis in higher eukaryotes, the aim is the reduction of the chromosome number from diploid to haploid (from 2n to n) in the nucleus of the gametes. In the present thesis, we have analysed the processes of synapsis and recombination in three species of mammals: humans, cats and dogs. - Content of the research: For the analysis of synapsis and recombination in three species of mammals (humans, cats and dogs) the immunocytogenetic technique has been used. It allowed to determine the quantitative values and the qualitative characteristics of these processes. - Conclusion: Infertility attributable to alterations in processes of recombination and chromosomal synapsis in autosomes and the sexual body is restricted to those individuals who present extreme deviations from the control range of these parameters. There is a recurrent meiotic phenotype characterized by an arrest in the zygotene to pachytene transition. The application of NGS techniques (exome analysis) in this infertile individual has allowed to locate a mutation in the TEX11 gene, probably pathogenic and responsible for the characteristics associated with this phenotype. The analysis of the relationship of the allelic variants of the PRDM9 gene with fertility problems and generation of de novo syndromes did not detect a significant association in any case. The influence of the RNF212 gene on the interindividual variability of recombination observed in the present study is associated with the presence of a genetic polymorphisms in that gene. Thus, each copy of the T allele in the SNP rs3796619 of this gene implies a mean decrease in the recombination rate of 132.5 cM compared to the C allele. There is a complex relationship between the PRDM9 genotypes and the rate of recombination, which appears to be determined by the length of the alleles, by the homozygosity or heterozygosity, and by dominance effects. There is significant intraindividual variability of the quantitative and qualitative aspects of recombination and synapsis in the three species analysed. This variability suggests that, in mammals, these processes and the factors controlling them must be flexible enough to generate diversity, albeit within margins that guarantee genomic stability. Significant differences have been observed in recombination processes between humans and cats. Thus, in cats the absence of recombination peaks has been determined in the subtelomeric regions, a lower inhibitory effect of the centromere and a more uniform distribution along the chromosome arms. These last two observations are related to the lower interference observed in this species. Synaptic characteristics of male cats, not previously described, have been observed. These include the presence of a reservoir of SYCP3 protein from leptotene to initial pachytene, premature separation of lateral elements from late pachytene or the changing morphology of the sexual body, which, as in humans, may be associated with the substage of this meiotic phase. Synaptic abnormalities have been detected in humans, cats and dogs, although the incidence of asynapsis, gaps and MSUC varied between species. In addition, the MSUC phenomenon has been described for the first time in these three species in individuals without chromosomal alterations of wild populations. In the sexual body, SYCP1 protein has been detected beyond the PAR region in the three species analysed. This presence could be related to a default polymerization process of SYCP1 protein, which would aid in the repair of DSBs located on the X chromosome.
Livres sur le sujet "RNF216"
Koizumi, Akio, Kazuhiro Nagata, Kiyohiro Houkin, Teiji Tominaga, Susumu Miyamoto, Shigeo Kure et Elizabeth Tournier-Lasserve, dir. Moyamoya Disease Explored Through RNF213. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2711-6.
Texte intégralNagata, Kazuhiro, Teiji Tominaga, Akio Koizumi, Kiyohiro Houkin, Susumu Miyamoto, Shigeo Kure et Elizabeth Tournier-Lasserve. Moyamoya Disease Explored Through RNF213 : Genetics, Molecular Pathology, and Clinical Sciences. Springer, 2018.
Trouver le texte intégralNagata, Kazuhiro, Teiji Tominaga, Akio Koizumi, Kiyohiro Houkin et Susumu Miyamoto. Moyamoya Disease Explored Through RNF213 : Genetics, Molecular Pathology, and Clinical Sciences. Springer, 2017.
Trouver le texte intégralNagata, Kazuhiro, Teiji Tominaga, Akio Koizumi, Kiyohiro Houkin, Susumu Miyamoto, Shigeo Kure et Elizabeth Tournier-Lasserve. Moyamoya Disease Explored Through RNF213 : Genetics, Molecular Pathology, and Clinical Sciences. Springer, 2017.
Trouver le texte intégralNagata, Kazuhiro, Akio Koizumi et Kiyohiro Houkin. Moyamoya Disease Explored Through RNF213 : Genetics, Molecular Pathology, and Clinical Sciences. Springer, 2017.
Trouver le texte intégralChapitres de livres sur le sujet "RNF216"
Nomura, Shunsuke, Hiroyuki Akagawa, Koji Yamaguchi, Akitsugu Kawashima et Takakazu Kawamata. « RNF213 and Clinical Feature ». Dans Moyamoya Disease : Current Knowledge and Future Perspectives, 61–72. Singapore : Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6404-2_5.
Texte intégralMorito, Daisuke, et Kazuhiro Nagata. « Molecular Biology of Mysterin/RNF213 ». Dans Current Topics in Environmental Health and Preventive Medicine, 45–57. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2711-6_4.
Texte intégralFujimura, Miki, Shigeo Kure et Teiji Tominaga. « Pathological Investigation on RNF213 : Animal Models of Rnf213-Knockout and Knock-in Mice ». Dans Current Topics in Environmental Health and Preventive Medicine, 79–89. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2711-6_7.
Texte intégralSharapova, Svetlana O. « RIDDLE Syndrome (RNF168) ». Dans Encyclopedia of Medical Immunology, 574–77. New York, NY : Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_160.
Texte intégralSharapova, Svetlana O. « RIDDLE Syndrome (RNF168) ». Dans Encyclopedia of Medical Immunology, 1–4. New York, NY : Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-9209-2_160-1.
Texte intégralKoizumi, Akio, et Shohab Youssefian. « A Prologue to Moyamoya Disease and RNF213 ». Dans Current Topics in Environmental Health and Preventive Medicine, 3–12. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2711-6_1.
Texte intégralMorito, Daisuke, et Kazuhiro Nagata. « Physiological Role of Mysterin/RNF213 in Zebrafish ». Dans Current Topics in Environmental Health and Preventive Medicine, 59–67. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2711-6_5.
Texte intégralMineharu, Yohei, Yasushi Takagi et Susumu Miyamoto. « Significance of RNF213 in Clinical Management in Japan ». Dans Current Topics in Environmental Health and Preventive Medicine, 137–50. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2711-6_11.
Texte intégralZhang, Zheng-Shan, et Lian Duan. « Significance of RNF213 in Clinical Management in China ». Dans Current Topics in Environmental Health and Preventive Medicine, 151–59. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2711-6_12.
Texte intégralKure, Shigeo. « Future Clinical Perspectives on RNF213 in Moyamoya Disease ». Dans Current Topics in Environmental Health and Preventive Medicine, 179–85. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2711-6_15.
Texte intégralActes de conférences sur le sujet "RNF216"
Zhi, Xu, Dong Zhao, Zhongmei Zhou et Ceshi Chen. « Abstract 213 : RNF126 E3 ubiquitin ligase targets p21cipfor ubiquitin-mediated degradation ». Dans Proceedings : AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012 ; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-213.
Texte intégralWang, Ying, Ou Deng, Zhihui Feng, Zhanwen Du, Xiahui Xiong, Ceshi Chen, Zhefu Ma et Junran Zhang. « Abstract 3013 : RNF126 promotes homologous recombination via regulating E2F1-mediated BRCA1 expression ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3013.
Texte intégralGuppy, Brent J., et Kirk J. McManus. « Abstract A02 : PARP inhibition selectively kills RNF20-depleted cells ». Dans Abstracts : AACR Precision Medicine Series : Synthetic Lethal Approaches to Cancer Vulnerabilities - May 17-20, 2013 ; Bellevue, WA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.pms-a02.
Texte intégralZhao, Hongchang, Min Zhu et Xingzhi Xu. « Abstract 2409 : BCL10 regulates RNF8/RNF168-mediated ubiquitination in the DNA damage response ». Dans Proceedings : AACR Annual Meeting 2014 ; April 5-9, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2409.
Texte intégralZhu, Qianzheng, Nidhi Sharma, Jingshan He, Gulzar Wani et Altaf A. Wani. « Abstract 3860 : USP7 deubiquitinase promotes ubiquitin-dependent DNA damage signaling by stabilizing RNF168 ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3860.
Texte intégralOrthwein, Alexandre, et Daniel Durocher. « Abstract IA12 : Regulation of the RNF168-dependent response to DNA double-strand breaks ». Dans Abstracts : AACR Special Conference : Cancer Susceptibility and Cancer Susceptibility Syndromes ; January 29-February 1, 2014 ; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.cansusc14-ia12.
Texte intégralCole, Alexander J., Kristie-Ann Dickson, Roderick Clifton-Bligh et Deborah J. Marsh. « Abstract 3538 : Targeting the E3 ubiquitin ligase RNF20 in ovarian cancer ». Dans 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.am2018-3538.
Texte intégralKorff, C., E. Ranza, X. Blanc, F. Santoni et S. Antonarakis. « Encephalopathy with Epilepsy and Movement Disorder Related to RNF13 : Case Report ». Dans Abstracts of the 48th Annual Meeting of the SENP (Société Européenne De Neurologie Pédiatrique). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1746215.
Texte intégralBanh, Robert S., Caterina Iorio, Richard Marcotte, Yang Xu, Dan Cojocari, Anas Abdel Rahman, Judy Pawling et al. « Abstract LB-302 : PTP1B regulates the Moyamoya disease-associated E3 ligase, RNF213 and cellular dioxygenase activity to allow breast tumor survival in hypoxia ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-302.
Texte intégralNie, Meng, Yongsheng Huang et Lin Wang. « Abstract 5328 : RNF12 inhibits the proliferation of hepatocellular carcinoma through c-Myc and p21 ». Dans 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.am2017-5328.
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