Gotowa bibliografia na temat „Tumstatin”
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Artykuły w czasopismach na temat "Tumstatin"
Wang, Shu Jing, Jia Liu, Fei Wang, Ning Chen, Shan Jiang, Lin Liu, Ying Zhao i Xiao Dan Zhang. "Tumstatin 7 Peptide Affect Biological Activity of B16 Melanoma Cell". Advanced Materials Research 641-642 (styczeń 2013): 915–18. http://dx.doi.org/10.4028/www.scientific.net/amr.641-642.915.
Pełny tekst źródłaBonn, Dorothy. "Tumstatin hints at how angiogenesis inhibitors work". Lancet Oncology 3, nr 2 (luty 2002): 71. http://dx.doi.org/10.1016/s1470-2045(02)00641-1.
Pełny tekst źródłaWANG, WEI, CHUN-XIAO XU, GUO-SHENG HOU, YOU-GEN CHEN, JIA-XUAN XIN i XIAN-XI LIU. "Downregulation of tumstatin expression by overexpression of ornithine decarboxylase". Oncology Reports 30, nr 5 (29.08.2013): 2042–48. http://dx.doi.org/10.3892/or.2013.2708.
Pełny tekst źródłaMaeshima, Y. "Tumstatin, an Endothelial Cell-Specific Inhibitor of Protein Synthesis". Science 295, nr 5552 (4.01.2002): 140–43. http://dx.doi.org/10.1126/science.1065298.
Pełny tekst źródłaOruc, Y., i S. Aydin. "Blood and aqueous humor tumstatin concentrations associated with diabetic retinopathy". Annals of Systems Biology 3, nr 1 (25.04.2020): 025–28. http://dx.doi.org/10.17352/asb.000008.
Pełny tekst źródłaNissen, Gyde, Henrike Hollaender, Francesca S. M. Tang, Michael Wegmann, Lars Lunding, Christina Vock, Anna Bachmann i in. "Tumstatin fragment selectively inhibits neutrophil infiltration in experimental asthma exacerbation". Clinical & Experimental Allergy 48, nr 11 (28.08.2018): 1483–93. http://dx.doi.org/10.1111/cea.13236.
Pełny tekst źródłaGu, Quliang, Tianyuan Zhang, Jinxian Luo i Fangyu Wang. "Expression, purification, and bioactivity of human tumstatin from Escherichia coli". Protein Expression and Purification 47, nr 2 (czerwiec 2006): 461–66. http://dx.doi.org/10.1016/j.pep.2006.01.011.
Pełny tekst źródłaCaudroy, Stephanie, Joel Cucherousset, Marianne Lorenzato, Jean-Marie Zahm, Corinne Martinella-Catusse, Myriam Polette i Philippe Birembaut. "Implication of tumstatin in tumor progression of human bronchopulmonary carcinomas". Human Pathology 35, nr 10 (październik 2004): 1218–22. http://dx.doi.org/10.1016/j.humpath.2004.06.008.
Pełny tekst źródłaXu, Chun-xiao, Xian-xi Liu, Guo-sheng Hou, Yun-fei Yan, Shi-min Chen, Wei Wang, Guang-shui Jiang, Bin Liu i Jia-xuan Xin. "The expression of tumstatin is down-regulated in renal carcinoma". Molecular Biology Reports 37, nr 5 (18.08.2009): 2273–77. http://dx.doi.org/10.1007/s11033-009-9718-9.
Pełny tekst źródłaWei, C., A. Y. Xun, X. X. Wei, J. Yao, J. Y. Wang, R. Y. Shi, G. H. Yang i in. "BifidobacteriaExpressing Tumstatin Protein for Antitumor Therapy in Tumor-Bearing Mice". Technology in Cancer Research & Treatment 15, nr 3 (11.05.2015): 498–508. http://dx.doi.org/10.1177/1533034615581977.
Pełny tekst źródłaRozprawy doktorskie na temat "Tumstatin"
Harkness, Louise Margaret. "The role of tumstatin in the asthmatic airway". Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/15416.
Pełny tekst źródłaBoustany, Sarah. "Mechanisms of Airway Remodelling". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3577.
Pełny tekst źródłaBoustany, Sarah. "Mechanisms of Airway Remodelling". University of Sydney, 2008. http://hdl.handle.net/2123/3577.
Pełny tekst źródłaAsthma is an inflammatory disease characterised by tissue remodelling. A prominent feature of this remodelling is an increase in the number and size of the blood vessels- formed from pre-existing capillaries – angiogenesis (Siddiqui et al., 2007; Wilson, 2003). This is triggered by many different endogenous angiogenic stimulators such as vascular endothelial growth factor (VEGF), and inhibited by endogenous angiogenic inhibitors such as tumstatin. Tumstatin is the non-collagenous domain (NC1) of the collagen IV α3 chain which, when cleaved, inhibits endothelial cell proliferation and induces apoptosis. Experiments described in this thesis have for the first time demonstrated the absence of tumstatin in the airways of individuals with asthma and lymphangioleiomyomatosis (LAM) as well as the functional responses to tumstatin as an angiogenic inhibitor, both in vitro and in vivo, in the airway. Although tumstatin was absent from the airways of asthmatic and LAM individuals it was present in the airways of individuals with no airways disease, chronic obstructive pulmonary disease, bronchiectasis and cystic fibrosis. No significant difference was seen in the levels of the Goodpasture Binding Protein (GPBP), a phosphorylating protein responsible for the alternate folding of tumstatin, between asthmatic, LAM and individuals with no airways disease. The αvβ3 integrin, reported to be necessary for the activity of tumstatin, as well as the individual αv and β3 sub-units were shown to be equally expressed in the airways of all patient groups. Co-localisation of tumstatin, VEGF and the αvβ3 integrin was seen in the disease free airways, however, a different pattern of VEGF and the αvβ3 integrin expression was observed in asthmatic and LAM airways with minimal co-localisation. Tumstatin was detected in serum and bronchoalveolar lavage fluid (BAL-f) samples from asthmatics and individuals with no airway disease, however there was no significant difference in the level of expression between the two groups. It was demonstrated that the tumstatin detected in the serum and BAL-f samples from asthmatics and individuals with no airway disease was part of the whole collagen IV α3 chain and not in its free and potentially active form. The ability of recombinant tumstatin to inhibit tube formation and proliferation of primary pulmonary endothelial cells was demonstrated for the first time. Further, the functional response of tumstatin was demonstrated in vivo in a mouse model of allergic airway disease. Tumstatin inhibited angiogenesis in the airway and decreased airway hyperresponsiveness. Whether there is potential for tumstatin, or a derivative thereof, to be of therapeutic value in airways diseases in which angiogenesis is a component should be the subject of future studies.
Streszczenia konferencji na temat "Tumstatin"
Harkness, Louise M., Anthony Ashton, Brian Oliver i Janette K. Burgess. "The Anti-Angiogenic Function Of Tumstatin In The Asthmatic Lung". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2410.
Pełny tekst źródłaGrafton, Karryn T., Janette K. Burgess, Lyn M. Moir, Judith Black i Brian G. Oliver. "Proteases May Cause The Loss Of Tumstatin From The Airways Of Asthmatics". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2076.
Pełny tekst źródłaWeckmann, Markus, Maree Svolos, Sarah Boustany, Brian G. Oliver, Janette K. Burgess, Lyn M. Moir i Judith Black. "Lamstatin And Tumstatin - Novel Inhibitors Of Lymphatic Cell Proliferation Are Absent In Lymphangioleiomyomatosis". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2093.
Pełny tekst źródłaWang, Shu-jing, Xing-han Liu, Yu-bin Ji i Ning Chen. "The Effect of Tumstatin Anti-tumor Peptide on Proliferation and Apoptosis of Different Cells". W 2007 1st International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/icbbe.2007.35.
Pełny tekst źródłaBurgess, Janette K., Karryn Grafton, Gavin Tjin, Josephine Middelburg, Pleun van Egmond, Judith L. Black i Brian G. Oliver. "The Role Of Cathepsin D In The Regulation Of Tumstatin Levels In Asthmatic Airways". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5341.
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