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    Wyświetlanie 1-4 z 4
    Tytuł:
    Conventional calpains and programmed cell death
    Autorzy:
    Łopatniuk, Paulina
    Witkowski, Jacek
    Powiązania:
    https://bibliotekanauki.pl/articles/1039875.pdf
    Data publikacji:
    2011
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    neurodegeneration
    calpain
    cancer
    apoptosis
    Opis:
    The evidence on the crucial role of a family of calcium-dependent cysteine proteases called calpains in programmed cell death is rich and still growing. However, understanding of the mechanisms of their functions in apoptosis is not full yet. Calpains have been implicated in both physiological and pathological cell death control, especially in various malignancies, but also in the immune system development and function. There is also growing evidence on calpain involvement in apoptosis execution in certain pathological conditions of the central nervous system, in cardiovascular diseases, etc. Understanding of the clinical significance of calpain activation pathways, after intense studies of the influence of calpain activity on drug-induced apoptosis, seems especially important lately, as calpains have become noticed as potential therapeutic targets. To allow pharmacological targeting of these enzymes, thorough knowledge of their patterns of activation and further interactions with already known apoptotic pathways is necessary. A comprehensive summary of both well established and recently obtained information in the field is an important step that may lead to future advances in the use of calpain-targeted agents in the clinic.
    Źródło:
    Acta Biochimica Polonica; 2011, 58, 3; 287-296
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Melatonin as an antioxidant: biochemical mechanisms and pathophysiological implications in humans.
    Autorzy:
    Reiter, Russel
    Tan, Dun-xian
    Mayo, Juan
    Sainz, Rosa
    Leon, Josefa
    Czarnocki, Zbigniew
    Powiązania:
    https://bibliotekanauki.pl/articles/1043401.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    neurodegeneration
    respiratory distress
    melatonin
    sepsis
    free radicals
    antioxidant enzymes
    antioxidant
    Opis:
    This brief resume enumerates the multiple actions of melatonin as an antioxidant. This indoleamine is produced in the vertebrate pineal gland, the retina and possibly some other organs. Additionally, however, it is found in invertebrates, bacteria, unicellular organisms as well as in plants, all of which do not have a pineal gland. Melatonin's functions as an antioxidant include: a), direct free radical scavenging, b), stimulation of antioxidative enzymes, c), increasing the efficiency of mitochondrial oxidative phosphorylation and reducing electron leakage (thereby lowering free radical generation), and 3), augmenting the efficiency of other antioxidants. There may be other functions of melatonin, yet undiscovered, which enhance its ability to protect against molecular damage by oxygen and nitrogen-based toxic reactants. Numerous in vitro and in vivo studies have documented the ability of both physiological and pharmacological concentrations to melatonin to protect against free radical destruction. Furthermore, clinical tests utilizing melatonin have proven highly successful; because of the positive outcomes of these studies, melatonin's use in disease states and processes where free radical damage is involved should be increased.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 4; 1129-1146
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Quality control in tRNA charging - editing of homocysteine
    Autorzy:
    Jakubowski, Hieronim
    Powiązania:
    https://bibliotekanauki.pl/articles/1039906.pdf
    Data publikacji:
    2011
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    tRNA synthetase editing
    homocysteine
    protein synthesis
    protein modification
    cardiovascular disease
    neurodegeneration
    Opis:
    All living organisms conduct protein synthesis with a high degree of accuracy maintained in the transmission and flow of information from a gene to protein product. One crucial 'quality control' point in maintaining a high level of accuracy is the selectivity by which aminoacyl-tRNA synthetases furnish correctly activated amino acids, attached to tRNA species, as the building blocks for growing protein chains. When differences in binding energies of amino acids to an aminoacyl-tRNA synthetase are inadequate, editing is used as a major determinant of enzyme selectivity. Some incorrect amino acids are edited at the active site before the transfer to tRNA (pre-transfer editing), while others are edited after transfer to tRNA at a separate editing site (post-transfer editing). Access of natural non-protein amino acids, such as homocysteine, homoserine, or ornithine to the genetic code is prevented by the editing function of aminoacyl-tRNA synthetases. Disabling editing function leads to tRNA mischarging errors and incorporation of incorrect amino acids into protein, which is detrimental to cell homeostasis and inhibits growth. Continuous homocysteine editing by methionyl-tRNA synthetase, resulting in the synthesis of homocysteine thiolactone, is part of the process of tRNA aminoacylation in living organisms, from bacteria to man. Excessive homocysteine thiolactone synthesis in hyperhomocysteinemia caused by genetic or nutritional deficiencies is linked to human vascular and neurological diseases.
    Źródło:
    Acta Biochimica Polonica; 2011, 58, 2; 149-163
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Genetic study of familial cases of Alzheimers disease.
    Autorzy:
    Kowalska, Anna
    Pruchnik-Wolińska, Danuta
    Florczak, Jolanta
    Modestowicz, Renata
    Szczech, Józef
    Kozubski, Wojciech
    Rossa, Grzegorz
    Wender, Mieczysław
    Powiązania:
    https://bibliotekanauki.pl/articles/1043353.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    neurodegeneration
    dementia
    presenilin 1 gene
    amyloid precursor protein gene
    Alzheimer's disease
    mutation
    presenilin 2 gene
    Opis:
    A small number (1-5%) of Alzheimer's disease (AD) cases associated with the early-onset form of the disease (EOAD) appears to be transmitted as a pure genetic, autosomal dominant trait. To date, three genes responsible for familial EOAD have been identified in the human genome: amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2). Mutations in these genes account for a significant fraction (18 to 50%) of familial cases of early onset AD. The mutations affect APP processing causing increased production of the toxic Aβ42 peptide. According to the "amyloid cascade hypothesis", aggregation of the Aβ42 peptide in brain is a primary event in AD pathogenesis. In our study of twenty AD patients with a positive family history of dementia, 15% (3 of 20) of the cases could be explained by coding sequence mutations in the PS1 gene. Although a frequency of PS1 mutations is less than 2% in the whole population of AD patients, their detection has a significant diagnostic value for both genetic counseling and treatment in families with AD.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 1; 245-242
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-4 z 4

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