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Książki na temat „Endoplasmic reticulum stress”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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Sprawdź 18 najlepszych książek naukowych na temat „Endoplasmic reticulum stress”.

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1

Agostinis, Patrizia, and Samali Afshin, eds. Endoplasmic Reticulum Stress in Health and Disease. Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9.

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2

Wagner, Cameron. Endoplasmic Reticulum Stress: Regulation, Function and Role in Health and Disease. Nova Science Publishers, Incorporated, 2016.

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Zhang, Kezhong, ed. Endoplasmic Reticulum Stress Response and Transcriptional Reprogramming. Frontiers SA Media, 2015. http://dx.doi.org/10.3389/978-2-88919-436-0.

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Agostinis, Patrizia, and Samali Afshin. Endoplasmic Reticulum Stress in Health and Disease. Springer Netherlands, 2014.

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Agostinis, Patrizia, and Samali Afshin. Endoplasmic Reticulum Stress in Health and Disease. Springer London, Limited, 2012.

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Endoplasmic Reticulum Stress In Health And Disease. Springer, 2012.

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Schäfer, Patrick, Lorenzo Frigerio, Federica Brandizzi, and Stephen H. Howell, eds. Endoplasmic reticulum - shape and function in stress translation. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-344-8.

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8

So, Jonathan. Characterization of the endoplasmic reticulum stress response in bipolar-I disorder. 2006.

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9

Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier, 2020. http://dx.doi.org/10.1016/c2019-0-04102-7.

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10

Madkour, Loutfy H. Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier Science & Technology Books, 2020.

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Madkour, Loutfy H. Reactive Oxygen Species , Nanoparticles, and Endoplasmic Reticulum Stress-Induced Cell Death Mechanisms: Antioxidant Therapeutic Defenses. Elsevier Science & Technology, 2020.

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Z.Y. Luo, Q. Song, X.P. Xiong, et al. The PI3K/Akt/mTOR signaling pathway regulates lipid metabolism mediated by endoplasmic reticulum stress in goose primary hepatocytes. Verlag Eugen Ulmer, 2021. http://dx.doi.org/10.1399/eps.2021.325.

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13

The unfolded protein response und cellular stress. Elsevier, 2011.

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14

Siebert, Stefan, Sengupta Raj, and Alexander Tsoukas. The genetics of axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0004.

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Family and twin studies have long suggested a large genetic component in ankylosing spondylitis (AS). The genetic association with HLA-B27 remains one of the strongest single gene variant associations reported in any complex polygenic disease. The exact mechanism by which HLA-B27 contributes to AS remains unknown, with three main theories proposed: the arthritogenic peptide, endoplasmic reticulum stress with unfolded protein response, and homodimerization theories. Genome-wide association studies have identified a number of other important susceptibility genes for AS, several of which overlap

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15

Colbert, Robert A., and Paul Bowness. Immune mechanisms: HLA-B27. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0006.

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HLA-B27 is present in the majority of patients with ankylosing spondylitis (AS). Although we have learned a considerable amount about the natural immunologic function of HLA class I proteins, this has not provided a definitive mechanism of AS pathogenesis. While HLA-B27 is adept at presenting antigenic peptides to CD8+ T cells, ‘arthritogenic’ peptides targeted by a cross-reactive T or natural killer cell response have not been described, nor have autoreactive T cells been found. Newer concepts have evolved based on the propensity of HLA-B27 to ‘misbehave’, both inside cells and on the cell su

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16

Raju, Raghavan, and Irshad H. Chaudry. The host response to hypoxia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0305.

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The hypoxic response of the host is complex. While the oxygen-sensing intracellular machinery attempts to restore cellular homeostasis by augmenting respiration and blood flow, events such as severe haemorrhage lead to whole body hypoxia and decreased mitochondrial function. Immunological perturbations following severe haemorrhage may result in multiple organ dysfunction and sepsis, while impaired perfusion may lead to microvascular injury and local hypoxia. Trauma-haemorrhage or hypoxic exposure in animals causes a systemic inflammatory response, decreased antigen presentation by peritoneal m

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Nakamura, Tomohiro, and Stuart A. Lipton. Neurodegenerative Diseases as Protein Misfolding Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0002.

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Neurodegenerative diseases (NDDs) often represent disorders of protein folding. Rather than large aggregates, recent evidence suggests that soluble oligomers of misfolded proteins are the most neurotoxic species. Emerging evidence points to small, soluble oligomers of misfolded proteins as the cause of synaptic dysfunction and loss, the major pathological correlate to disease progression in many NDDs including Alzheimer’s disease. The protein quality control machinery of the cell, which includes molecular chaperones as found in the endoplasmic reticulum (ER), the ubiquitin-proteasome system (U

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18

Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease

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