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Artykuły w czasopismach na temat "P14ARF"
Cilluffo, Danilo, Viviana Barra i Aldo Di Leonardo. "P14ARF: The Absence that Makes the Difference". Genes 11, nr 7 (20.07.2020): 824. http://dx.doi.org/10.3390/genes11070824.
Pełny tekst źródłaEymin, Béatrice, Paule Claverie, Caroline Salon, Camille Leduc, Edwige Col, Elisabeth Brambilla, Saadi Khochbin i Sylvie Gazzeri. "p14ARF Activates a Tip60-Dependent and p53-Independent ATM/ATR/CHK Pathway in Response to Genotoxic Stress". Molecular and Cellular Biology 26, nr 11 (1.06.2006): 4339–50. http://dx.doi.org/10.1128/mcb.02240-05.
Pełny tekst źródłaHe, Mingwei, Jinlei Pang, Haiyan Sun, Guanrong Zheng, Yan Lin i Weipeng Ge. "P14ARF inhibits regional inflammation and vascularization in intervertebral disc degeneration by upregulating TIMP3". American Journal of Physiology-Cell Physiology 318, nr 4 (1.04.2020): C751—C761. http://dx.doi.org/10.1152/ajpcell.00271.2019.
Pełny tekst źródłaShamanin, Vladimir A., i Elliot J. Androphy. "Immortalization of Human Mammary Epithelial Cells Is Associated with Inactivation of the p14ARF-p53 Pathway". Molecular and Cellular Biology 24, nr 5 (1.03.2004): 2144–52. http://dx.doi.org/10.1128/mcb.24.5.2144-2152.2004.
Pełny tekst źródłaCho, E. Y., Y. L. Choi, S. W. Chae, J. H. Sohn i G. H. Ahn. "Relationship between p53-associated proteins and estrogen receptor status in ovarian serous neoplasms". International Journal of Gynecologic Cancer 16, nr 3 (2006): 1000–1006. http://dx.doi.org/10.1136/ijgc-00009577-200605000-00008.
Pełny tekst źródłaSánchez-Aguilera, Abel, Margarita Sánchez-Beato, Juan F. Garcı́a, Ignacio Prieto, Marina Pollan i Miguel A. Piris. "p14ARF nuclear overexpression in aggressive B-cell lymphomas is a sensor of malfunction of the common tumor suppressor pathways". Blood 99, nr 4 (15.02.2002): 1411–18. http://dx.doi.org/10.1182/blood.v99.4.1411.
Pełny tekst źródłaOlcha, Piotr, Marek Cybulski, Danuta Skomra, Bogdan Obrzut, Atanas Ignatov, Maciej Jóźwik, Regine Schneider-Stock i Andrzej Semczuk. "The Pattern of p14ARF Expression in Primary and Metastatic Human Endometrial Carcinomas". International Journal of Gynecologic Cancer 20, nr 6 (lipiec 2010): 993–99. http://dx.doi.org/10.1111/igc.0b013e3181e76a4d.
Pełny tekst źródłaSong, Joon Seon, Joo Mi Yi, Hanbyoul Cho, Chel Hun Choi, Yoonho Park, Eun Joo Chung, Jaewhan Song, Joon-Yong Chung i Seung-Mo Hong. "Dual loss of USP10 and p14ARF protein expression is associated with poor prognosis in patients with small intestinal adenocarcinoma". Tumor Biology 40, nr 10 (30.10.2018): 101042831880867. http://dx.doi.org/10.1177/1010428318808678.
Pełny tekst źródłaMartinez, Juan Carlos, Santiago Ropero, Concepcion Mateos, Maria DEL VAL Toledo, Rafael Samaniego, Silvia Sacristan i Manel Esteller. "Alteration of the p53 and Rb tumor suppressor pathways by p16/INK4a and p14/ARF promoter methylation and loss of protein expression in recurrent and nonrecurrent meningiomas." Journal of Clinical Oncology 31, nr 15_suppl (20.05.2013): 2064. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.2064.
Pełny tekst źródłaBai, Ming, Nan-Ze Yu, Fei Long, Cheng Feng i Xiao-Jun Wang. "Effects of CDKN2A (p16INK4A/p14ARF) Over-Expression on Proliferation and Migration of Human Melanoma A375 Cells". Cellular Physiology and Biochemistry 40, nr 6 (2016): 1367–76. http://dx.doi.org/10.1159/000453189.
Pełny tekst źródłaRozprawy doktorskie na temat "P14ARF"
Müer, Annika [Verfasser]. "Funktionelle Charakterisierung des p14ARF-Tumorsuppressorsignalwegs / Annika Müer". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/1029792585/34.
Pełny tekst źródłaAbraham, Aswin George. "Nucleophosmin and p14ARF mediated regulation of p53". Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:06e101f9-f0e3-42b9-ada9-7a1b1a1f4a87.
Pełny tekst źródłaLindström, Mikael. "Functional characterization of the alternative reading frame protein p14ARF /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-917-x.
Pełny tekst źródłaCarr-Wilkinson, Jane. "Inactivation of the p53/MDM2/p14ARF pathway in neuroblastoma". Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.515033.
Pełny tekst źródłaMistry, Sushilaben Harkisandas. "The role of p14ARF in familial and sporadic melanoma". Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413193.
Pełny tekst źródłaDayde, Delphine. "Liens fonctionnels entre l'EGFR et P14ARF : contribution à la carcinogenèse pulmonaire". Thesis, Grenoble, 2014. http://www.theses.fr/2014GRENV071/document.
Pełny tekst źródłaEGFR is a transmembrane tyrosine kinase (TK) receptor which activates proliferative and survival signals. In lung cancer, its activity is frequently deregulated by overexpression and/or mutation in its TK domain. These mutations are mainly of two types (L858R and Del19) and are called « driver mutations » because they induce constitutive activation of EGFR oncogenic signaling. They also represent a predictive responsive factor to EGFR TKIs that specifically inhibit this receptor. P14ARF is a tumor suppressor that restricts cellular proliferation and maintains genomic stability. We described its inactivation in lung cancer and demonstrated that its expression inhibits their development. Our recent results show that the expression of p14ARF is inhibited in a majority of lung adenocarcinomas expressing an activating EGFR mutation. Based on these results we hypothesized that inhibition of p14ARF expression contributes to clonal expansion of mutated EGFR-bearing tumor. P14ARF could be a break to EGFR oncogenic activity.In different models of lung adenocarcinoma expressing a L858R EGFR mutant we show that transient expression of p14ARF activates a pro-apoptotic STAT3/Bcl-2-dependent signaling pathway. In turn, EGFR inhibits the expression of p14ARF and blocks its pro-apoptotic function. We also show that EGFR (wild type or mutated) activation inhibits the expression of p14ARF at the transcriptional level. This implies a nuclear translocation of EGFR controlled by Class III PI3K (Vps34) and its fixation to the ARF promoter. This work identifies for the first time a functional link between EGFR and p14ARF signaling pathways. They highlight a new mechanism of tumor progression by which a nuclear EGFR signaling inactivates the tumor suppressor p14ARF to allow tumor growth
Gallagher, Stuart John. "The Role of the p14ARF Tumour Suppressor in Promoting Apoptosis". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3597.
Pełny tekst źródłaGallagher, Stuart John. "The Role of the p14ARF Tumour Suppressor in Promoting Apoptosis". University of Sydney, 2008. http://hdl.handle.net/2123/3597.
Pełny tekst źródłaThe incidence of melanoma has risen dramatically during the past three decades, yet there has been little improvement in effective treatments for this intractable and aggressive disease. Melanoma tumours are notoriously resistant to apoptosis, a cell suicide program that is activated by most cancer therapies. This thesis explores the role of the melanoma susceptibility gene product p14ARF in promoting cell cycle arrest and apoptosis, in order to resolve the impact of this tumour suppressor in melanomagenesis and melanoma susceptibility. The p14ARF tumour suppressor gene is mutated in almost half of all cancers, and germline mutations in p14ARF confer a greatly increased risk of developing melanoma. The primary function of p14ARF is to relay oncogenic signals to p53, a central regulator of cellular response to stress. There is conflicting evidence regarding the role of p14ARF in promoting apoptosis. Much of the current evidence is based on murine studies, which may not translate accurately to humans due to important differences in animal physiology and the primary sequence and functions of the mouse and human ARF proteins. Furthermore, results from previous studies are often compounded by supra-physiological expression of p14ARF, and are complicated by the fact that p14ARF shares its genomic sequence with the p16INK4a tumour suppressor gene. This study demonstrates that p14ARF expression in human cancer and primary cell lines promotes rapid p53-dependent cell cycle arrest, rather than apoptosis. As p14ARF expression did not induce apoptosis, we investigated if p14ARF could modulate the sensitivity of a cell to apoptosis induced by cytotoxic agents. Using a p14ARF-inducible U2OS osteosarcoma cell line model, we examined the impact of p14ARF expression on the apoptotic response of the cell to a panel of thirteen cytotoxic agents. p14ARF expression increased apoptosis caused by a sub-set of agents, including trichostatin A, sodium butyrate, DRB, Adriamycin and UVB radiation. p14ARF-mediated chemosensitivity was p53- and caspase-dependent, and involved the loss of mitochondrial potential. While loss of mitochondrial potential was dependent on p53, it was not blocked by caspase inhibition, demonstrating that caspases play a role downstream of mitochondrial depolarisation. Inhibition of individual components of the apoptotic program showed that p14ARF-mediated chemosensitivity was not strictly dependent on the pro-apoptotic Bax or Fas proteins. We also investigated whether p14ARF could sensitise melanoma to chemotherapeutics in vivo. We investigated the expression level of p14ARF, p16INK4a and MITFm and mutation status of B-RAF, N-RAS and PTEN in melanomas from 30 patients that had undergone isolated limb infusion - a palliative therapeutic strategy that results in much higher response rates than systemic treatment. Expression of p14ARF did not predict response to the drugs actinomycin D and melphalan . Instead, high expression of p16INK4a and presence of activating N-RAS mutation were independent predictors of response to high doses of these chemotherapeutic drugs. This work suggests that p14ARF analogues may be beneficial adjuncts in cancer therapy, but are unlikely to be effective as single agents. Additionally, p14ARF mimetics will only be effective in tumours with intact p53 signalling. Melanomas frequently carry functional p53, and may be susceptible to this mode of treatment providing the apoptotic pathway downstream of p53 is intact or can be restored.
Andrique, Laetitia. "Nouveaux partenaires du suppresseur de tumeurs p14ARF : découverte de nouvelles fonctions indépendantes de p53". Poitiers, 2007. http://www.theses.fr/2007POIT1403.
Pełny tekst źródłaStraza, Michael W. "A Tale of Two ARFs: Tumor Suppressor and Anti-viral Functions of p14ARF: A Dissertation". eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/472.
Pełny tekst źródłaKsiążki na temat "P14ARF"
Stewart, Craig Leslie. p53-independent growth arrest of human astrocytomas by p14arf. Ottawa: National Library of Canada, 2000.
Znajdź pełny tekst źródłaIvanchuk, Stacey M. Identification and characterization of novel p14ARF tumour suppressor binding partners. 2005.
Znajdź pełny tekst źródłaCzęści książek na temat "P14ARF"
"p14ARF". W Encyclopedia of Cancer, 3347. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_101738.
Pełny tekst źródła"P14ARF". W Encyclopedia of Cancer, 2739. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4322.
Pełny tekst źródła"ARF (ADP-ribosylation factor, p14ARF [human]/p19ARF[mouse])". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 140. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_1117.
Pełny tekst źródłaGazzeri, Sylvie, i Elisabeth Brambilla. "Immunohistochemical Expression of E2F1 and p14ARF in Lung Carcinoma". W Handbook of Immunohistochemistry and in Situ Hybridization of Human Carcinomas, 133–39. Elsevier, 2002. http://dx.doi.org/10.1016/s1874-5784(04)80024-2.
Pełny tekst źródłaKonishi, Noboru. "9 Role of the p14ARF and p16INK4a Genes in Prostate Cancer". W Molecular Pathology, Colorectal Carcinoma, and Prostate Carcinoma, 369–76. Elsevier, 2002. http://dx.doi.org/10.1016/s1874-5784(02)80041-1.
Pełny tekst źródłaStreszczenia konferencji na temat "P14ARF"
Lwanga, Robert, John R. Horton i Xiaodong Cheng. "The Arginine Methylation of P14ARF". W The MD Anderson Summer Experience 2022. The University of MD Anderson Cancer Center, 2022. http://dx.doi.org/10.52519/00032.
Pełny tekst źródłaMudryj, Maria, Salma Siddiqui, Stephen J. Libertini, Alan P. Lombard, Benjamin Mooso, Leandro D'Abronzo, Frank Melgoza i in. "Abstract 5051: Androgen receptor-mediated regulation of p14ARF transcription in prostate tumor cells". W 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.am2015-5051.
Pełny tekst źródłaSoni, Nikita, Shine Devarajan i Nikhil Gadewal. "The effect of p14ARF and YY1 peptides in MDM2-p53 mediated oncogenic pathway: An in silico perspective". W 2018 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2018. http://dx.doi.org/10.1109/bsb.2018.8770613.
Pełny tekst źródłaBoothello, Rio S., Nirmita J. Patel, Priyadarshan K. Damle, Chetna Sharon, Kranthi Kumar Chougoni, Umesh R. Desai, Steven R. Grossman i Bhaumik B. Patel. "Abstract 3460: p38-p14ARF-CtBP2 axis as a novel regulator of CSC phenotype and tumor cell dormancy". W 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.am2018-3460.
Pełny tekst źródłaShi, Xu-Bao, Sumaira Amir, Ai-Hong Ma, Lingru Xue i Ralph W. deVere White. "Abstract 3056: miR-125b suppresses p14ARF and modulates p53-dependent and p53-independent apoptosis in prostate cancer cells." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3056.
Pełny tekst źródłaSong, Joon Seon, Hanbyoul Cho, Joon-Yong Chung, Ilseon Hwang, Hee Jin Lee, Seung-Mo Hong i Stephen M. Hewitt. "Abstract 5729: Loss of USP10 and p14ARF protein expression is associated with poor prognosis patients with small intestinal adenocarcinoma". W 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.am2017-5729.
Pełny tekst źródłaCerqueira, Otto Luiz, Maria Alejandra Salomon, Elaine Cristina Cardoso, Tharcisio Citrangulo Tortelli i Bryan Eric Strauss. "Abstract 5548: Indicators of immune activation upon p14ARF and interferon-beta gene transfer in a human melanoma cell line". W Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5548.
Pełny tekst źródłaCisneros, J., M. Checa, B. Ortiz-Quintero, V. Ruiz, M. Negreros, JS Hagood, A. Pardo i M. Selman. "Hypermethylation Mediated Silencing of p14ARF in Fibroblasts from Patients with Idiopathic Pulmonary Fibrosis (IPF): A Putative Role in Fibroblasts Resistance to Apoptosis." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3481.
Pełny tekst źródłaZoppoli, Gabriele M., William C. Reinhold, Stephanie Solier, Anne Monks, John W. Connelly, Hongfang Liu, Kurt W. Kohn, Robert Shoemaker i Yves Pommier. "Abstract 1103: Linkage between endogenous Chk2 activation and p14ARF expression in p53-mutated cells revealed by proteomic and genomic analyses of the NCI60". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1103.
Pełny tekst źródłaMcGowan, E., N. Alling, R. Shephard, D. Yagoub, N. Tran i P. Xia. "Abstract P1-04-03: A Role for Cyclin D1 in Neoplastic Transformation in MCF-7 Breast Cancer Cells Post p14ARF-p53 Induced Senescence". W Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p1-04-03.
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