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Books on the topic 'Proteasome System'

Author: Grafiati

Published: 23 September 2022

Last updated: 28 September 2022

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1

Mayor, Thibault, and Gary Kleiger, eds. The Ubiquitin Proteasome System. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8706-1.

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2

name, No. The ubiquitin-proteasome proteolytic system: From classical biochemistry to human diseases. Singapore: World Scientific, 2002.

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3

Rechsteiner, Martin, Aaron J. Ciechanover, and R. John Mayer. Ubiquitin-Proteasome System. Wiley & Sons, Incorporated, John, 2008.

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4

Rechsteiner, Martin, Aaron J. Ciechanover, and R. John Mayer. Ubiquitin-Proteasome System. Wiley & Sons, Limited, John, 2008.

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5

Ciechanover, Aaron J., and Maria G. Masucci. The Ubiquitin-Proteasome Proteolytic System. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/5051.

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6

Rechsteiner, Martin, Aaron J. Ciechanover, and R. John Mayer. Ubiquitin-Proteasome System and Disease. Wiley & Sons, Incorporated, John, 2008.

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7

(Editor), Leonidas Stefanis, and J. N. Keller (Editor), eds. The Proteasome in Neurodegeneration. Springer, 2006.

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8

The Ubiquitin Proteasome System: Methods and Protocols. Humana, 2018.

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9

Rechsteiner, Martin, Aaron J. Ciechanover, and R. John Mayer. Cell Biology of the Ubiquitin-Proteasome System. Wiley & Sons, Incorporated, John, 2008.

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10

Mayer, J., and R. Layfield. The Ubiquitin-proteasome System (Essays in Biochemistry). Portland Pr, 2005.

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11

(Editor), R. John Mayer, Aaron J. Ciechanover (Editor), and Martin Rechsteiner (Editor), eds. Protein Degradation: The Ubiquitin-Proteasome System (Protein Degradation). Wiley-VCH, 2006.

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12

Gomes, Aldrin V. Ubiquitin Proteasome System: A Review and Directions for Research. Nova Science Publishers, Incorporated, 2018.

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13

Rechsteiner, Martin, Aaron J. Ciechanover, and R. John Mayer. Cell Biology of the Ubiquitin-Proteasome System Vol. 3. Wiley & Sons, Limited, John, 2007.

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14

(Editor), Mario Di Napoli, and Cezary Wojcik (Editor), eds. The Ubiquitin Proteasome System in the Central Nervous System: From Physiology to Pathology. Nova Science Pub Inc, 2008.

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15

(Editor), R. John Mayer, Aaron J. Ciechanover (Editor), and Martin Rechsteiner (Editor), eds. Protein Degradation: Cell Biology of the Ubiquitin-Proteasome System (Protein Degradation). Wiley-VCH, 2006.

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16

Summers, Matthew, ed. Ubiquitin Proteasome System - Current Insights into Mechanism Cellular Regulation and Disease. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.78430.

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17

(Editor), Aaron J. Ciechanover, and Maria G. Masucci (Editor), eds. The Ubiquitin-Proteasome Proteolytic System: From Classical Biochemistry to Human Diseases. World Scientific Publishing, 2003.

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18

J, Ciechanover Aaron, and Masucci Maria G, eds. The ubiquitin-proteasome proteolytic system: From classical biochemistry to human diseases. Singapore: World Scientific, 2002.

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19

Di, Napoli Mario, and Wójcik Cezary 1968-, eds. The ubiquitin proteasome system in the central nervous system: From physiology to pathology : 2008 update. Hauppauge, NY: Nova Science, 2009.

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20

(Editor), R. John Mayer, Aaron J. Ciechanover (Editor), and Martin Rechsteiner (Editor), eds. Protein Degradation: Vol. 4: The Ubiquitin-Proteasome System and Disease (Protein Degradation). Wiley-VCH, 2007.

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21

Renton, Alan E., and Alison M. Goate. Genetics of Dementia. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0051.

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Abstract:

The genetic architecture of dementia is polygenic and complex, with risk alleles spanning frequency–effect size space. Despite significant progress, most genes influencing these disorders await discovery. Known risk loci implicate perturbed pathways that coalesce around recurring mechanistic themes, notably the autophagosome-lysosome system, the cytoskeleton, endocytosis, innate immunity, lipid metabolism, mitochondria, and the ubiquitin-proteasome system. Phenotypic and pathophysiological pleiotropy suggests some conditions form continuous clinicopathogenetic disease spectra blurring classical diagnoses. Future large-scale genome sequencing of global populations will significantly elucidate etiopathogenesis and is likely to reframe nosology. Furthermore integrative prospective cohort studies have the potential to revolutionize our understanding of dementia.

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22

Grune, Tilman. Proteasomal System in Aging and Disease. Elsevier Science & Technology Books, 2012.

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23

The Proteasomal System in Aging and Disease. Elsevier, 2012. http://dx.doi.org/10.1016/c2010-0-66760-5.

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24

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 (UPS), and various forms of autophagy, can counterbalance the accumulation of misfolded proteins to some extent. Their ability to eliminate the neurotoxic effects of misfolded proteins, however, declines with age. A plausible explanation for the age-dependent deterioration of the quality control machinery involves compromise of these systems by excessive generation of reactive oxygen species (ROS), such as superoxide anion (O2-), and reactive nitrogen species (RNS), such as nitric oxide (NO). The resulting redox stress contributes to the accumulation of misfolded proteins. Here, we focus on aberrantly increased generation of NO-related species since this process appears to accelerate the manifestation of key neuropathological features, including protein misfolding. We review the chemical mechanisms of posttranslational modification by RNS such as protein S-nitrosylation of critical cysteine thiol groups and nitration of tyrosine residues, showing how they contribute to the pathogenesis of NDDs.

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25

Purintrapiban, Juntipa. Coordination of protease systems on muscle protein degradation and identification of calpain substrates using the yeast two-hybrid system. 1999.

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26

Hodgkiss, Andrew. Psychiatric consequences of cancer treatments: ‘small molecule’ molecularly targeted agents. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0008.

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The psychiatric consequences of a range of small-molecule, molecularly targeted systemic treatments for cancer are reviewed. Psychopathology may arise from the endocrine complications of VEGFR/multiple TK inhibitors. The mechanisms by which PI3K/AKT inhibition and proteasome inhibition can provoke anxiety and depressive phenomena in animals and humans are discussed. PARP-1 inhibition impairs memory acquisition in animal models and is neuroprotective. PARP-2 inhibitors display anti-neuroinflammatory properties in mice. The cognitive enhancing, mood stabilizing, and neuroprotective effects of HDAC inhibitors are considered.

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27

Kanno, Hiroshi, and Joachim P. Steinbach. Familial tumour syndromes: von Hippel–Lindau disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0016.

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Von Hippel–Lindau (VHL) disease, an autosomal dominant familial tumour syndrome, is often associated with haemangioblastoma of the central nervous system. In the presence of oxygen, VHL protein serves to prevent the accumulation of hypoxia-inducible factor (HIF) protein by targeting it to the proteasomal pathway, while biallelic inactivation of the VHL gene blocks degradation of HIF and leads to constitutive activation of the HIF pathway although oxygen is present. HIF-target genes are involved in angiogenesis, proliferation, and metabolism enabling tumour growth. Haemangioblastoma is a highly vascularized, begin tumour commonly associated with a cyst, but it is linked with neurological morbidity and mortality based on its location and multiplicity. Haemangioblastoma in VHL is diagnosed according to symptoms and signs, past and family histories, laboratory data, neuroradiological findings, pathological findings, and genetic testing. Surgical treatment is usually the most recommended therapy for haemangioblastomas, and using well-defined microsurgical techniques, the majority can be resected safely.

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28

Berry, Martin, and Ann Logan. CNS Injuries: Cellular Responses and Pharmacological Strategies (Pharmacology & Toxicology (Crc Pr)). CRC, 1998.

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29

M, Berry, and Logan Ann, eds. CNS injuries: Cellular responses and pharmacological strategies. Boca Raton: CRC Press, 1999.

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