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Libros sobre el tema "Human proteases"

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Autor: Grafiati
Publicado: 14 de marzo de 2023

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1

Chakraborti, Sajal, Tapati Chakraborti y Naranjan S. Dhalla, eds. Proteases in Human Diseases. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3162-5.

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2

Cheronis, John Chris Dion, 1951- y Repine John E, eds. Proteases, protease inhibitors, and protease-derived peptides: Importance in human pathophysiology and therapeutics. Basel: Birkhäuser Verlag, 1993.

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3

West, A. Investigations by mass spectrometry of the interactions of novel serine protease inhibitors with Herpes Simplex Virus type 2 and Human Cytomegalovirus proteases. [s.l.]: typescript, 1999.

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4

Genesio, Murano, ed. Protease inhibitors of human plasma: Biochemistry and pathophysiology. Westbury, N.Y: PJD Publications, 1986.

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5

Massimi, Isabella. SspB cysteine protease of Staphylococcus aureus promotes detachment of human keratinocytes and degrades fibronectin and vitronectin. Ottawa: National Library of Canada, 2001.

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6

John Chris Dion Cheronis (Editor) y John E. Repine (Editor), eds. Proteases, Protease Inhibitors & Proteasederived Peptides : Importance in Human... Birkhauser Boston, 1993.

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7

Dhalla, Naranjan S., Sajal Chakraborti y Tapati Chakraborti. Proteases in Human Diseases. Springer, 2018.

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8

Dhalla, Naranjan S., Sajal Chakraborti y Tapati Chakraborti. Proteases in Human Diseases. Springer, 2017.

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9

Dhalla, Naranjan S., Sajal Chakraborti y Tapati Chakraborti. Proteases in Human Diseases. Springer, 2017.

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10

Dhalla, Naranjan S., Sajal Chakraborti y Tapati Chakraborti. Proteases in Human Diseases. Springer, 2017.

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11

Cheronis, J. y Repine. Proteases, Protease Inhibitors and Protease-Derived Peptides: Importance in Human Pathophysiology and Therapeutics. Birkhäuser Boston, 2012.

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12

Turner, Robert T. The complete catalytic specificity of the human aspartic proteases, memapsin 1 and mepapsin 2 (β-secreatase). [s.n.], 2002.

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13

Frontiers in Research of the Renin-Angiotensin System on Human Disease (Proteases in Biology and Disease). Springer, 2008.

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14

Murano, Genesio. Protease Inhibitors of Human Plasma Biochemistry and Pathophysiology (Protease Inhibitors of Human Plasma-Biochemistry & Pathophys). P J D Publications, Limited, 1985.

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15

Smith, Stephanie J., Rohini J. Manuel y Christopher C. Kibbler. Aspergillus species. Editado por Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum y Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0010.

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There are more than 200 Aspergillus species, with over 30 known to be human pathogens. The fungus is also commercially important. Aspergillus niger is the source of enzymes such as amylases, lipases, and proteases and is used to produce the majority of the world’s citric acid. Diseases caused by Aspergillus species can vary widely, from superficial colonization to invasive and allergic disease. Mortality from invasive disease remains high, despite an increase in the number of antifungals available for therapy. Azole resistance is increasing, especially in Europe, and appears to be related to the use of azoles for agriculture.
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16

Zerovnik, Eva. Human Stefins And Cystatins. Nova Biomedical Books, 2006.

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17

Liu, Fenyong. The human herpes simplex virus I protease and its substrate, the capsid scaffolding protein. 1993.

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18

Michel, Jean-Baptiste. Biology of vascular wall dilation and rupture. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0016.

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Arterial pathologies, important causes of death and morbidity in humans, are closely related to modifications in the circulatory system during evolution. With increasing intraluminal pressure and arterial bifurcation density, the arterial wall becomes the target of interactions with blood components and outward convection of plasma solutes and particles, including plasma zymogens and leukocyte proteases. Abdominal aortic aneurysms of atherothrombotic origin are characterized by the presence of an intraluminal thrombus (ILT), a major source of proteases, including plasmin, MMP-9, and elastase. Saccular cerebral aneurysms are characterized by the interaction of haemodynamics and arterial bifurcation defects, of either genetic or congenital origin. They also develop an intrasaccular thrombus, implicated in rupture. Aneurysms of the ascending aorta (TAAs) are not linked to atherothrombotic disease, and do not develop an ILT. The most common denominator of TAAs, whatever their aetiology, is the presence of areas of mucoid degeneration, and increased convection and vSMC-dependent activation of plasma zymogens within the wall, causing extracellular matrix proteolysis. TAA development is also associated with an epigenetic phenomenon of SMAD2 overexpression and nuclear translocation, potentially linked to chronic changes in mechanotransduction. Aortic dissections share common aetiologies and pathology (areas of mucoid degeneration) with TAAs, but differ by the absence of any compensatory epigenetic response. There are main experimental animal models of aneurysms, all characterized by the cessation of aneurysmal progression after interruption of the exogenous stimuli used to induce it. These new pathophysiological approaches to aneurysms in humans pave the way for new diagnostic and therapeutic tools.
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19

Livingston, Schuyler, Benjamin Young, Martin Markowitz, Poonam Mathur y Bruce L. Gilliam. HIV Virology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0017.

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HIV is a member of the lentivirus subfamily of retroviruses. Two distinct groups of viruses are pathogenic in humans: HIV-1 and HIV-2. Both are transmitted sexually and known to cause immunodeficiency disease. HIV enters the cell through use of the CD4 receptor and chemokine co-receptors, primarily CCR5 and CXCR4. The viral genome is transcribed from RNA to DNA by reverse transcriptase and integrated into the host genome by integrase. The HIV genome encodes 15 proteins, comprising three categories: structural, regulatory, and accessory. After budding from the host cell, the virus matures into its infectious form through cleavage of viral precursor proteins by protease.
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