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Статті в журналах з теми "C-Cdh1"
Ross, Karen E., and Orna Cohen-Fix. "The Role of Cdh1p in Maintaining Genomic Stability in Budding Yeast." Genetics 165, no. 2 (October 1, 2003): 489–503. http://dx.doi.org/10.1093/genetics/165.2.489.
Повний текст джерелаAlkebsi, Lobna A., Hiroshi Handa, Kenichi Tahara, Hiroaki Shimizu, Takuma Ishizaki, Kunio Yanagisawa, Makiko Takizawa, et al. "Chromosome 16q Located Genes CDH1, CDH13 and ADAMTS18 Are Correlated and Frequently Methylated But Not Associated With DNMTs levels In Human Lymphoma." Blood 122, no. 21 (November 15, 2013): 4289. http://dx.doi.org/10.1182/blood.v122.21.4289.4289.
Повний текст джерелаQiao, Xinxian, Liyong Zhang, Armin M. Gamper, Takeo Fujita, and Yong Wan. "APC/C-Cdh1." Cell Cycle 9, no. 19 (October 2010): 3904–12. http://dx.doi.org/10.4161/cc.9.19.13585.
Повний текст джерелаHöckner, Sebastian, Lea Neumann-Arnold, and Wolfgang Seufert. "Dual control by Cdk1 phosphorylation of the budding yeast APC/C ubiquitin ligase activator Cdh1." Molecular Biology of the Cell 27, no. 14 (July 15, 2016): 2198–212. http://dx.doi.org/10.1091/mbc.e15-11-0787.
Повний текст джерелаListovsky, Tamar, and Julian E. Sale. "Sequestration of CDH1 by MAD2L2 prevents premature APC/C activation prior to anaphase onset." Journal of Cell Biology 203, no. 1 (October 7, 2013): 87–100. http://dx.doi.org/10.1083/jcb.201302060.
Повний текст джерелаArnold, Lea, Sebastian Höckner, and Wolfgang Seufert. "Insights into the cellular mechanism of the yeast ubiquitin ligase APC/C-Cdh1 from the analysis of in vivo degrons." Molecular Biology of the Cell 26, no. 5 (March 2015): 843–58. http://dx.doi.org/10.1091/mbc.e14-09-1342.
Повний текст джерелаYanjun, Xu, Cao Wenming, Xu Qi, Guo Jianmin, Wang Xinbao, Cheng Xiangdong, and Ying Jieer. "Searching for CDH1 gene mutations in early-onset diffuse gastric cancer in Chinese patients." Journal of Clinical Oncology 32, no. 3_suppl (January 20, 2014): 23. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.23.
Повний текст джерелаMartinez, Juan S., Dah-Eun Jeong, Eunyoung Choi, Brian M. Billings, and Mark C. Hall. "Acm1 Is a Negative Regulator of the Cdh1-Dependent Anaphase-Promoting Complex/Cyclosome in Budding Yeast." Molecular and Cellular Biology 26, no. 24 (October 9, 2006): 9162–76. http://dx.doi.org/10.1128/mcb.00603-06.
Повний текст джерелаKrohs, Julika, Dominik Schnerch, Marie Follo, Julia Felthaus, Monika Engelhardt, and Ralph M. Waesch. "The Tumor Suppressor APC/CCdh1 and Its Role In Replication Stress and The Origin Of Genomic Instability." Blood 122, no. 21 (November 15, 2013): 2489. http://dx.doi.org/10.1182/blood.v122.21.2489.2489.
Повний текст джерелаSchmidts, Andrea, Dagmar Wider, Julia Felthaus, Manuel Hein, Dominik Schnerch, Monika Engelhardt, and Ralph M. Waesch. "APC/C-Cdh1 as a Novel Regulator of Hematopoietic Stem Cell Differentiation." Blood 116, no. 21 (November 19, 2010): 1563. http://dx.doi.org/10.1182/blood.v116.21.1563.1563.
Повний текст джерелаДисертації з теми "C-Cdh1"
Belahmer, Hanane [Verfasser]. "APC/C Cdh1 modulates the ER stress response via Gadd34 / Hanane Belahmer." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2011. http://d-nb.info/1021438804/34.
Повний текст джерелаAlves, Carlos Eduardo Fonseca. "Avaliação epigenética dos genes NKX3.1 E CDH1 e expressão do C-MYC, NKX3.1 e E-Caderina por imuno-histoquímica em microarranjo de tecido (TMA) de lesões pré-neoplásicas e neoplásicas na próstata de cães." Botucatu, 2016. http://hdl.handle.net/11449/143108.
Повний текст джерелаResumo: A próstata canina é um bom modelo para estudos comparados entre o cão e o homem, uma vez que essas duas espécies desenvolvem espontaneamente carcinoma de próstata (CP). Para melhor caracterização do CP canino, a presente pesquisa foi dividia em quatro capítulos que avaliam diferentes aspectos dos CPs em cães. A atrofia inflamatória proliferativa (PIA) é uma lesão pré-neoplásica descritas em humanos e pouco estuda em cães. Nós caracterizamos essa lesão em cães e identificamos uma forte relação entre a localização topográfica da PIA com os CPs. Além disso, foi identificada a perda de expressão gênica e proteica de PTEN e AR na PIA. Esses fatores associados corroboram com o potencial pré-neoplásico desta lesão em cães. Um achado interessante foi a alta expressão de P63 na PIA e em um grupo de CP caninos. Para melhor caracterizar este grupo, foi avaliada a expressão imuno-histoquímica de diferentes citoqueratinas e outras proteínas relacionadas ao desenvolvimento do CP em humanos. Os carcinomas que apresentam expressão de P63 apresentaram padrões morfológicos com escore de Gleason alto e um fenótipo mais agressivo quando comparado à tumores que não apresentação expressão de P63. Posteriormente, a expressão gênica e proteica de E-caderina, NKX3.1 e C-MYC foi avaliada em CP como marcadores nas diferentes lesões. Além disso, nós avaliamos a metilação como mecanismo regulatórios dos genes CDH1 e NKX3.1. Foi possível identificar a perda de E-caderina e NKX3.1 nos tumores, comparado à ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The canine prostate gland can be used as a model to human prostatic disease since dogs and men are the only species that spontaneously develop prostate carcinoma (PC). To better characterize the canine PC, this research was divided into four chapters that evaluated different aspects of the PC in dogs. The proliferative inflammatory atrophy (PIA) is a pre-neoplastic lesion described in humans and few studies in dogs describe it as a preneoplastic lesion. This study characterized PIA in dogs and identified a strong relationship between the PIA topography with PC. In addition, we identified the loss of PTEN and AR expression in PIA. These findings demonstrated the potential of PIA as a preneoplastic lesion in dogs. An interesting finding in this research was the high expression of P63 in PIA and a group of PC. This study found a group of PC showing P63 positive expression in neoplastic epithelial cells. Thus, these tumors were selected to better characterize them using immunohistochemistry. These tumors had an aggressive phenotype and presented high expression of AKT and C-MYC and loss of NKX3.1. Further, we selected a usual group of PC and evaluate the expression of E-cadherin, NKX3.1 and C-MYC. In addition, we evaluated the methylation as a regulatory mechanism of CDH1 and NKX3.1 genes. We have identified loss of E-cadherin and NKX3.1 in PC compared to normal prostate and C-MYC overexpression. The expression of E-cadherin was related to overall survival and Gleason score. The ... (Complete abstract click electronic access below)
Doutor
Cataldo, Francesca. "Role of calpain in USP1 stability regulation and genome integrity maintenance." Doctoral thesis, Università degli studi di Trieste, 2012. http://hdl.handle.net/10077/7860.
Повний текст джерелаThe calpains are a family of intracellular cysteine proteases, among which the best studied isoforms, micro- (CAPN1) and milli-calpain (CAPN2), are heterodimers consisting of a catalytic subunit and a common regulatory subunit, CAPNS1, required for function. Calpain is involved in many processes important for cancer biology, such as autophagy, indeed in calpain-depleted cells autophagy is impaired, with a subsequent increase in apoptosis sensitivity. Calpain is also important in all the stages of the stress response. A proteomic approach was employed for the identification of novel CAPNS1 interacting proteins. Proteins immunoprecipitating with endogenous CAPNS1 in HT1080 cell lysates were analyzed by Mass Spectrometry. We identified novel partners among which the deubiquitinating enzyme USP1, a key regulator of the DNA damage response and genome integrity maintenance via its specific action on FANCD2, involved in DNA repair and protection from chromosome instability, and PCNA, involved in the regulation of translesion DNA synthesis (TLS), that bypasses DNA lesions with low stringency basepairing requirements. We performed co-IP assays in lysates of 293T cells and confirmed that the interaction was specific. Furhermore, we observed that calpain is able to bind a USP1 C-terminal deleted mutant, suggesting that USP1 first 523 aminoacids were sufficient for the binding. To understand what is the effect exerted by calpain upon USP1, we depleted calpain activity in a series of cell lines, and followed the fate of endogenous USP1. We transfected CAPNS1 specific siRNAs, or treated cells with a specific inhibitor of calpain, and we observed a strong decrease in USP1 protein levels. This effect should be at a post-transcriptional level, since any significant change in USP1 mRNA levels is detected. We also obtained the same result by transfecting a siRNA specific for CAPN1, the gene encoding for the catalytic subunit micro-calpain. Moreover, we studied the role of calpain in the PCNA-mediated switch between high fidelity replication and TLS upon UV irradiation. In mouse embryonic fibroblasts knockout for CAPNS1, USP1 downregulation is coupled to an increase in PCNA monoubiquitination. Moreover, CAPNS1-depleted U2OS cells showed an increase in the percentage of nuclei containing PCNA-induced foci upon UV irradiation. Since we demonstrated that calpain can modulate an important regulator of DNA damage response such as USP1, we investigated if calpain could have a role in genome integrity maintenance. CAPNS1 depleted cells showed a reduced rescue in DNA repair compared to control cells, suggesting that increased levels in PCNA monoubiquitination could lead to an increased amount of errore-prone TLS. Calpain plays an important role in autophagy, so we asked if USP1 degradation in absence of calpain activity could involve autophagic pathways. We first blocked macroautophagy by silencing ATG5, and we observed that USP1 was downregulated, suggesting that the depletion of ATG5 could lead to an increased activity of other degradation pathways. To impaire chaperone-mediated autophagy (CMA), we silenced a protein important for autophagosome formation, LAMP-2A. Also in this case we observed a decrease in USP1 protein levels, thus suggesting that USP1 is alternatively degraded by different pathways. However, we observed that USP1 is stabilized upon inhibition of lysosomal enzymes, suggesting that USP1 may be degraded in the lysosome. To better understand the mechanism by which calpain affect USP1 stability we search for an effect of calpain upon USP1 co-factor and activator UAF1/WDR48. CAPNS1-depleted cells showed WDR48 downregulation, but WDR48 overexpression only partially rescue USP1 protein levels in this cells. Furthermore, we provided evidences that calpain regulation of p35/p25 activator of Cdk5 can affect Cdh1 phosphorylation and thus APC/Cdh1 activity, leading to a regulation of USP1 stabilization. In conclusion, we identified USP1 as a novel interactor of calpain, and we found that calpain is important for USP1 stability, since in its absence USP1 is downregulated. The importance of this novel regulation is strengthened by the recent findings that unveiled a role of USP1 in maintenance of a mesenchymal stem cell program in osteosarcoma, and thus placing calpain in a crucial regulatory position for cancer development.
XXIV Ciclo
1983
Timoteo, Ana Rafaela de Souza. "Identifica??o e caracteriza??o molecular de muta??es germinativas em indiv?duos com s?ndrome de c?ncer de mama e ov?rio heredit?rio." PROGRAMA DE P?S-GRADUA??O EM BIOQU?MICA, 2016. https://repositorio.ufrn.br/jspui/handle/123456789/22712.
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A S?ndrome de c?ncer de mama e ov?rio heredit?rio corresponde a 10-15% de todos os casos diagnosticados de c?ncer de mama no mundo. A maioria das muta??es germinativas s?o identificadas nos genes BRCA1 e BRCA2, contudo, a aplica??o de pain?is multig?nicos tem aumentado o n?mero de variantes patog?nicas detectadas em outros genes supressores de tumor. De acordo com a vers?o atual do protocolo americano NCCN (National Comprehensive Cancer Network), as muta??es em BRCA1 e BRCA2, TP53 e PTEN conferem alto risco de desenvolver c?ncer de mama, e muta??es em CDH1, CHEK2, PALB2, ATM e BRIP podem aumentar em 20% o risco para o desenvolvimento desta doen?a. Neste estudo foram analisados 157 indiv?duos com hist?rico pessoal e/ou familiar de c?ncer de mama. O DNA gen?mico foi isolado a partir de sangue perif?rico por meio de extra??o ? base de solu??o salina e as amostras foram analisadas usando o sequenciamento de nova gera??o (NGS). Foram identificadas 15 variantes patog?nicas e 4 VUS (Variants of Uncertain Significance) em 27 indiv?duos (27/157; 17%), dos quais tr?s s?o assintom?ticos. Foram identificadas sete novas variantes em 4 genes: BRCA1_c.3409A>G; BRCA2_g.26826_30318del, BRCA2_c.5800C>T; BRCA2_c.5228G>A; BRCA2_c.5305delG; ATM_c.634delT e ATR_c.3043C>T. Sessenta e oito por cento (13/19; 68%) de variantes foi detectada nos genes BRCA1 e BRCA2, enquanto 32% (6/19) foram identificados nos genes de risco moderado ATM (2/19); ATR (1/19); CDH1 (1/19); MLH1 (1/19) e MSH6 (1/19). Os indiv?duos foram separados em dois grupos para a an?lise comparativa: portadores de muta??o nos genes de alto risco e nos genes de risco moderado. Entre os tr?s indiv?duos assintom?ticos, duas variantes est?o presentes nos genes de risco moderado ATM e MLH1. Entre os indiv?duos com c?ncer de mama, dezoito pacientes (18/24; 75%) apresentaram muta??es em genes de alto risco, enquanto seis (6/24; 25%) s?o portadores de muta??es em genes de risco moderado. Ambos os grupos apresentaram alta incid?ncia de c?ncer de mama precocemente (83% dos indiv?duos). O grupo de portadores de muta??o nos genes de alto risco apresentaram maior ocorr?ncia de tumores de alto grau (83% vs 67%, P = 0,0090). No grupo de indiv?duos com muta??es em genes de risco moderado, os tumores apresentaram um fen?tipo mais agressivo com c?ncer bilateral (33% versus 11%, P = 0,0002), ocorr?ncia de met?stases (33% vs 5,6%, P <0,0001) e ?bito (33% vs 5,6%, P <0,0001). Ao todo, 1/3 de variantes foram identificadas em genes de risco moderado em pacientes com c?ncer mais agressivo. Estes resultados refor?am a import?ncia da aplica??o de an?lise multig?nica em indiv?duos em situa??o de risco para c?ncer de mama, especialmente em uma popula??o heterog?nea como brasileira.
Hereditary breast and ovarian cancer (HBOC) corresponds to 10-15% of all diagnosed cases of breast cancer in the world. The majority germline mutations are identified in BRCA1 and BRCA2 genes, however the application of multigene panels has increased the number of pathogenic variations detected in DNA repair genes. According to the current version of NCCN (National Comprehensive Cancer Network) Guideline, mutations in BRCA1, BRCA2, TP53 and PTEN confers high risk to develop breast cancer, and mutations in CDH1, CHEK2, PALB2, ATM and BRIP can increases over than 20% this risk. We analyzed 157 individuals with personal and/or familial breast cancer history. Genomic DNA was isolated from peripheral blood through saline-based extraction and samples were analyzed using next-generation sequencing (NGS). We identified 15 pathogenic variants and 4 VUS (Variants of Uncertain Significance) in 27 individuals (27/157; 17%), in which three are asymptomatic. Seven novel variants in 4 genes were identified: BRCA1_c.3409A>G; BRCA2_g.26826_30318del, BRCA2_c.5800C>T; BRCA2_c.5228G>A; BRCA2_c.5305delG; ATM_c.634delT and ATR_c.3043C>T. Sixty-eight percent (13/19; 68%) of variants was detected in BRCA1 and BRCA2 genes, while 32% (6/19) were identified in moderate risk genes ATM (2/19); ATR (1/19); CDH1 (1/19); MLH1 (1/19) and MSH6 (1/19). The individuals were separated in two groups for comparative analysis: high-risk genes and moderate risk genes. Among three asymptomatic individuals, two present variants in moderate risk genes ATM and MLH1. Among breast cancer individuals, eighteen patients (18/24; 75%) presented mutations in high-risk genes, while six (6/24; 25%) harbored mutations in moderate risk genes. Both groups had a high incidence of early-onset breast cancer, 83%. The group of individuals harboring variants in high-risk genes presented a greater occurrence of high-grade tumors (83% vs. 67%, P= 0.0090). In the group of individuals harboring mutation in moderate risk genes, tumors presented a more aggressive phenotype with bilateral cancer (33% vs. 11%, P= 0.0002), occurrence of metastasis (33% vs. 5.6%, P<0.0001) and incidence of deaths (33% vs. 5.6%, P<0.0001). Altogether, 1/3 of variants were identified in moderate risk genes in patients presenting a more aggressive phenotype. These results reinforce the importance of applying multigene analysis in individuals at-risk for breast cancer, especially in a heterogeneous population as Brazilian.
Kannan, Madhuvanthi. "The Role of the E3 Ubiquitin Ligase Cdh1-APC in Axon Growth in the Mammalian Brain." Doctoral thesis, 2012. http://hdl.handle.net/11858/00-1735-0000-000D-EF73-C.
Повний текст джерелаChou, Hsin-I. "The role of APC activators Cdc20p and Cdh1p in regulating mitosis and morphogenesis in C. albicans." Thesis, 2008. http://spectrum.library.concordia.ca/975925/1/MR45280.pdf.
Повний текст джерелаЧастини книг з теми "C-Cdh1"
Issa, Khalil, Abdulaziz Alanazi, Khalid A. Aldhafeeri, Ola Alamer, and Mazen Alshaaer. "Brushite: Synthesis, Properties, and Biomedical Applications." In Crystallization and Applications. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102007.
Повний текст джерелаТези доповідей конференцій з теми "C-Cdh1"
Масалимова, Минлегуль, та Альфия Нургалиева. "АНАЛИЗ РОЛИ ГЕНЕТИЧЕСКОГО ВАРИАНТА C.1320+1G>A ГЕНА CDH1 В РАЗВИТИИ РАКА ЖЕЛУДКА". У Фундаментальная математика и ее приложения в естествознании. Baskir State University, 2022. http://dx.doi.org/10.33184/fmpve2022-2022-10-19.217.
Повний текст джерелаBoer, Harmen R. de, Lorenzo Lafranchi, Christine Neugebauer, Rudolf S. N. Fehrmann, Elisabeth G. E. de Vries, Alessandro A. Sartori, and Marcel A. T. M. van Vugt. "Abstract 1315: CtIP is regulated by the APC/C-Cdh1 to mediate cell cycle-dependent control of DNA repair." In 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.am2014-1315.
Повний текст джерела