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Rozprawy doktorskie na temat „Calpain 2”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 13 lutego 2022

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1

Mendes, Atlante Silva. "Verapamil diminui a expressão proteica de calpaína-1 e metaloproteinase de matriz-2 na hipertrofia cardíaca induzida por hipertensão renovascular." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-08112018-150232/.

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Introdução: A hipertrofia cardíaca induzida por sobrecarga hemodinâmica crônica (HC) é caracterizada por espessamento das paredes do ventrículo esquerdo e do tecido intersticial. As atividades aumentadas de calpaína-1 e metaloproteinase de matriz(MMP)-2 são observadas em diferentes modelos de hipertensão arterial e estão relacionadas com as mudanças fisiopatológicas na HC. Por outro lado, a atividade de MMP-2 parece ser modulada positivamente por ativação de calpaína-1 em diferentes modelos. O objetivo deste trabalho é analizar se a calpaína-1 contribui para o aumento da atividade de MMP-2 no

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2

Breiden, Maike [Verfasser], Michael [Akademischer Betreuer] Ehrmann, and Markus [Akademischer Betreuer] Kaiser. "Charakterisierung der Interaktion von HTRA1 und Calpain 2 / Maike Breiden. Gutachter: Markus Kaiser. Betreuer: Michael Ehrmann." Duisburg, 2014. http://d-nb.info/1058323385/34.

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3

Howells, Anwen. "The impact of innate immune cells on immunopathology in dengue." Thesis, University of Oxford, 2014. https://ora.ox.ac.uk/objects/uuid:0a251372-4d0e-416d-ad3c-8e07e6729e1b.

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Dengue virus (DENV) is an arthropod-borne virus and has become a worldwide problem with steadily rising annual infection rates. Patients present with a range of symptoms from mild fever to, in some cases, life-threatening hemorrhagic fever and shock syndrome. The most severe cases require emergency hospital care and currently, there is no effective drug treatment or vaccine for dengue. As severe symptoms appear post-peak viremia, immuno-pathology is thought to be the cause and a potential trigger of this is differential activation of the immune response upon recognition of DENV. This could be

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4

Liu, Tongzheng. "Regulation of Inflammtory Activation in Endothelial Cells by PIN1." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1242756227.

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5

Stroop, Davis M. "The Epidemiology of Early Type 2 Diabetes Mellitus in Black and White Females: Genetic and Environmental Factors." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1377870493.

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6

Sanchez, Brualla Irene. "The potassium-chloride cotransporter KCC2 : a new therapeutic target for spasticity and neuropathic pain." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0677.

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La spasticité et la douleur neuropathique sont deux symptômes apparaissant fréquemment après une lésion médullaire. La spasticité est définie comme une augmentation du tonus musculaire qui provoque des contractures, tandis que la douleur neuropathique se caractérise par des sensations douloureuses survenant suite à une lésion du système nerveux.Ces deux symptômes résultent en partie d’une désinhibition des réseaux neuronaux sous-lésionnels lié à une diminution de l’expression du cotransporteur potassium-chlorure type 2 (KCC2). Pour être efficace,l’inhibition nécessite l’action de cette protéin

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7

Muir, Matthew Stewart. "Proteomics of the ovine cataract." Diss., Lincoln University, 2008. http://hdl.handle.net/10182/792.

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The lens of the eye needs to be completely transparent in order to allow all light entering the eye to reach the retina. This transparency is maintained by the highly ordered structure of the lens proteins the crystallins. Any disruption to the lens proteins can cause an opacity to develop which is known as cataract. During cortical cataract formation there is increased truncation of the lens crystallins. It is believed that overactivation of calcium-dependent cysteine proteases, the calpains, is responsible for the increased proteolysis of the crystallins seen during cataractogenesis. Within

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8

Ruppert, Anne-Marie. "Rôle des calpaïnes extracellulaires dans la progression des adénocarcinomes lépidiques." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066317/document.

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La calpaïne 1 est une protéase à cystéine activée par le calcium, qui peut être partiellement externalisée. Les calpaines extracellulaires favorisent la résolution de l'inflammation et la réparation des tissus, à travers la prolifération et la migration cellulaire. Le récepteur Toll like (TLR) 2 a été identifié comme une cible des calpaïnes extracellulaires dans les lymphocytes. L'objectif est d'étudier le rôle de la calpaïne extracellulaire 1 dans la progression tumorale de l'adénocarcinome pulmonaire lepidique (ADL). La calpaïne extracellulaire, le fragment soluble de TLR2, le versican et le

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9

Hanna, Rachel. "REGULATION OF CALPAIN 2 BY CALPASTATIN." Thesis, 2010. http://hdl.handle.net/1974/5639.

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Calpains are a family of intracellular cysteine proteases activated by calcium. They participate in many processes including cell motility, cell cycle progression and cell death, in response to calcium signaling. Because calpain over-activation as a result of calcium dysregulation is a contributing factor to many disease states, these enzymes are important therapeutic targets. Within the cell, calpains 1 and 2 are regulated by the protein inhibitor calpastatin. This unstructured protein is specific for calpain, binds tightly, and recognizes only the activated form of the enzyme. Detailed

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10

Lal, Sangeet Kumar. "Calpain 2 proteolysis regulates glioblastoma cell invasion." Thesis, 2010. http://hdl.handle.net/1957/19988.

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Glioblastoma is the most malignant primary brain tumor with the average patients surviving only one year after diagnosis, even with aggressive therapy. The formation of numerous micro-tumors dispersed into the brain due to rapid invasion of tumor cells, presents the primary challenge to the surgical removal of tumors and limits the effectiveness of current treatments. This dissertation presents studies aimed at understanding the molecular mechanisms regulating invasion of human glioblastoma cells. Transplantation of human glioblastoma cells in the zebrafish brain showed that the knockdown of c

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11

Chou, Jordan. "CALPAIN 2 ACTIVATION, AUTOLYSIS, AND SUBUNIT DISSOCIATION." Thesis, 2010. http://hdl.handle.net/1974/6172.

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Calpains are calcium-dependent, intracellular, multi-domain cysteine proteases involved in many physiological functions regulated by calcium signaling, including cell motility. How calpains are activated in the cell is still unknown because the resting intracellular concentration of Ca2+ is orders of magnitude lower than that needed for half-maximal activation of the enzyme in vitro. Several stratagems by which calpains might overcome this Ca2+ concentration differential have been proposed. It is possible that post-translational modifications like phosphorylation, or accessory proteins tha

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12

Wang, Hsueh-Chun, and 王雪君. "The regulation of calpain-2 activity bytyrosine phosphorylation and sumoylationThe regulation of calpain-2 activity by tyrosine phosphorylation and sumoylation." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/33230396816915184021.

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博士<br>國防醫學院<br>生命科學研究所<br>97<br>The calpain family of proteases are important for several key aspects of cell motility, including cell spreading, membrane protrusion, detachment of the rear and integrin, growth-factor-mediated signaling. The calpain activity can be activated by calcium, phospholipid binding, autolysis, serine phosphorylation

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13

Fromberg, Iris [Verfasser]. "Immunhistochemische Untersuchungen zur Expression von Calpain 1, Calpain 2 und Calpastatin in Endometrium- und Ovarialkarzinom / vorgelegt von Iris Fromberg." 2009. http://d-nb.info/1006602755/34.

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14

CHEN, Huan-Hsin, and 陳奐新. "The study of mouse -actinin 2 protein degradation mediated through calpain in the cytoplasmic localization." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/46093406023057710926.

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碩士<br>國防醫學院<br>生物化學研究所<br>97<br>Mouse alpha actinin 2 (mACTN2) belongs to the spectrin protein superfamily, which is composed of 894 residues and expresses in the heart, skeletal muscle, lung, and brain. Our previous study demonstrated that mACTN2 and its superfamily member contain LXXLL motif, the Nuclear receptor (NR) binding motif, and serve as a coactivator for nuclear receptor, mACTN2 also bind to the C-terminal region of GRIP1 (glucocorticoid receptor interacting protein 1) for the secondary nuclear receptor functions. Our previous study identified the NES (nuclear export signals) of mAC

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15

Kennedy, Michael Alex Ander. "Role of the caspase and calpain families in mediating pancreatic beta cell dysfunction and death in type 2 diabetes." Thesis, 2006. http://hdl.handle.net/2429/18279.

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Type 2 diabetes is characterized by an inability to maintain normoglycemia due to impairments in both insulin secretion and action. The impaired capacity of the pancreatic beta cell to secrete sufficient concentrations of insulin directly contributes to the worsening glycemic control. High concentrations of glucose and free fatty acids have been shown to be deleterious for pancreatic beta cell function and viability. Increased availability of glucose and free fatty acids may also contribute to the aggregation of islet amyloid polypeptide (IAPP) and formation of islet amyloid, a commonly observ

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16

Wang, Chia-Fang, and 王家芳. "Calpain 2 Activated through N-Methyl-D-Aspartic Acid Receptor Signaling Cleaves CPEB3 and Abrogates CPEB3-Repressed Translation in Neurons." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/06955054182621952272.

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博士<br>國防醫學院<br>生命科學研究所<br>101<br>Long-term memory requires the activity-dependent reorganization of the synaptic proteome to modulate synaptic efficacy and consequently consolidate memory. Activity-regulated RNA translation can change the protein composition at the stimulated synapse. Cytoplasmic polyadenylation element-binding protein 3 (CPEB3) is a sequence-specific RNA-binding protein that represses translation of its target mRNAs in neurons, while activation of N-methyl-D-aspartic acid (NMDA) receptors alleviates this repression. Although recent research has revealed the mechanism of CPEB3

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17

Chen, Huang-Hui. "Ca²⁺ and phosphoinositides regulations in α-actinin -4 F-actin binding". 2008. http://hdl.handle.net/2440/51019.

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α-actinin-4 is a non-muscle isoform of α-actinin that belongs to the spectrin superfamily. It comprises three functional regions: an N-terminal actin-binding region that consists of two calponin homology (CH) domains, a central region that consists of four copies of the spectrin-like repeat domain and a C-terminal calmodulin-like domain that is predicted to bind Ca²⁺. α-actinin-4 is organised as an antiparallel homodimer formed by the interaction of four spectrin-like repeats between the two monomers, giving a rod-like shape, with actin binding regions at both ends. α-actinin-4 is an abundant

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