Gotowe bibliografie tematyczne / Tumstatin

Gotowa bibliografia na temat „Tumstatin”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 21 lutego 2023

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Artykuły w czasopismach na temat "Tumstatin"

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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.

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To study the effect of biological activity of Tumstatin 7 peptide on the cell proliferation and apoptosis of B16 melanoma. Tumstatin 7 peptide was synthesized and its purity is 98.4532% by high-performance liquid chromatography. The effect of 7 peptide on B16 melanoma was observed by MTT, cell growth curve, the observation of the transmission electron microscope (TEM). 7 peptide can significantly inhibit B16 melanoma cell proliferation, showing dose- and time-dependent .Its IC50 was 72.53 μg/ml.The morphology of B16 melanoma cell was obviously changed by TEM, such as karyopyknosis and apoptotic bodies. So7 peptides can inhibit the proliferation of melanoma cells and promote melanoma cells apoptosis. It will be of great potential value to melanoma treatment.
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Bonn, 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.

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WANG, 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.

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Maeshima, 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.

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Oruc, 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.

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Nissen, 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.

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Gu, 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.

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Caudroy, 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.

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Xu, 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.

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Wei, 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.

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Rozprawy doktorskie na temat "Tumstatin"

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Harkness, Louise Margaret. "The role of tumstatin in the asthmatic airway". Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/15416.

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The extracellular matrix ECM is essentially the tissue microenvironment, orchestrating cell growth and behavior. An altered airway ECM has been implemented in many features of asthma pathophysiology. This thesis investigated properties of the ECM intrinsically deposited by asthmatic ASM cells to better understand factors driving altered protein deposition. This thesis also investigated the viability of the ECM microenvironment as a therapeutic target in asthma. In the presence of inflammatory stimuli asthmatic ASM cells are reported to deposit an ECM abnormal in composition and functionality. This thesis however revealed when all stimulation is removed these cells intrinsically deposit ‘healthy’ ECM the same in fibronectin and collagen I content and angiogenic potential as the non-asthmatic ASM-ECM, and suggest inflammatory stimuli may be driving the development and persistence of an irregular matrix. Unfortunately anti-inflammatory medications do not completely suppress airway inflammation in asthmatic individuals. This thesis thus explored additional alternative therapeutic avenues for the treatment of asthma. Tumstatin is a matrikine, reduced in asthma, which possesses asthma-resolving potential when administered in mouse models of asthma. This thesis revealed tumstatin utilises active MMPs to remodel the ECM from asthmatic ASM cells and establish an anti-inflammatory and anti-remodelling microenvironment. This thesis further demonstrates the therapeutic potential of tumstatin in an ‘asthmatic’ sheep model, resolving airway remodelling and eosinophilia in a pulmonary system closely representative of the human. This thesis revealed factors driving the altered ECM and therapeutic avenues to ‘normalise’ the ECM microenvironment for complete resolution of the asthmatic phenotype.
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Boustany, Sarah. "Mechanisms of Airway Remodelling". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3577.

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Asthma 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.
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Boustany, Sarah. "Mechanisms of Airway Remodelling". University of Sydney, 2008. http://hdl.handle.net/2123/3577.

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Doctor of Philosophy (PhD)
Asthma 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.
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Streszczenia konferencji na temat "Tumstatin"

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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.

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Grafton, 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.

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Weckmann, 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.

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Wang, 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.

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Burgess, 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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