https://transhumanist.ru/index.php?action=history&feed=atom&title=CASP5 2026-07-19T02:25:34Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=CASP5&diff=6046&oldid=prev 2021-05-12T15:08:27Z

<p>Новая страница: «Caspase-5 precursor (EC 3.4.22.58) (CASP-5) (ICE(rel)-III) (Protease ICH-3) (Protease TY) [Contains: Caspase-5 subunit p20; Caspase-5 subunit p10] [ICH3] ==Publi...»</p> <p><b>Новая страница</b></p><div>Caspase-5 precursor (EC 3.4.22.58) (CASP-5) (ICE(rel)-III) (Protease ICH-3) (Protease TY) [Contains: Caspase-5 subunit p20; Caspase-5 subunit p10] [ICH3]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Gene expression of inflammasome components in peripheral blood mononuclear cells (PBMC) of vascular patients increases with age.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26448778<br /> |abstract=Chronic low-grade inflammation is considered a driver of many age-related disorders, including vascular diseases (inflammaging). Inhibition of autophagic capacity with ageing was postulated to generate a pro-inflammatory condition via activation of inflammasomes, a group of Interleukin-1 activating intracellular multi-protein complexes. We thus investigated gene expression of inflammasome components in PBMC of 77 vascular patients (age 22-82) in association with age. Linear regression of real-time qRT-PCR data revealed a significant positive association of gene expression of each of the inflammasome components with age (Pearson correlation coefficients: [[AIM2]]: r = 0.245; P = 0.032; [[NLRP3]]: r = 0.367; P = 0.001; ASC (PYCARD): r = 0.252; P = 0.027; [[CASP1]]: r = 0.296; P = 0.009; [[CASP5]]: r = 0.453; P = 0.00003; [[IL1B]]: r = 0.247; P = 0.030). No difference in gene expression of [[AIM2]], [[NLRP3]], ASC [[CASP1]], and [[CASP5]] was detected between PBMC of patients with advanced atherosclerosis and other vascular patients, whereas [[IL1B]] expression was increased in PBMC of the latter group (P = 0.0005). The findings reinforce the systemic pro-inflammatory phenotype reported in elderly by demonstrating an increased phase-1 activation of inflammasomes in PBMC of vascular patients.<br /> <br /> |keywords=* AIM2<br /> * Aging<br /> * Atherosclerosis<br /> * Inflammation<br /> * NLRP3<br /> * Vascular disease<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4596365<br /> }}<br /> {{medline-entry<br /> |title=Evidence for depletion of [[CASP5]] Ala90Thr heterozygous genotype in aged subjects.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/20434535<br /> |abstract=Our previous studies, which included genotyping of multiple coding apoptotic gene polymorphisms, unexpectedly demonstrated a depletion of heterozygous [[CASP5]] Ala90Thr (rs507879, c.268 G&gt;A) genotypes in elderly subjects. Present investigation was aimed to validate this trend. An analysis of 510 subjects aged 75-103years revealed 205 (40%) [[CASP5]] Ala90Thr heterozygotes as compared to 254 (50%) expected from the minor allele frequency 0.470 (p=0.000014). This deviation was not observed in 549 middle-aged (18-50years) controls (270 (49%) heterozygotes observed vs. 274 (50%) expected; minor allele frequency 0.475; p=0.743). Unfavorable significance of [[CASP5]] heterozygous genotype may be explained by the role of the caspase-5 in inflammation-related processes. Almost all prior gene-longevity association studies focused on discrimination between &quot;good&quot; and &quot;bad&quot; gene variants. Here we present a distinct situation, where the combination of alternative alleles (i.e., heterozygosity) appears to be unfavorable as compared to the homozygous carriership of either gene variant.<br /> |mesh-terms=* Adolescent<br /> * Adult<br /> * Aged<br /> * Aged, 80 and over<br /> * Amino Acid Substitution<br /> * Apoptosis<br /> * Caspases<br /> * DNA Primers<br /> * Gene Frequency<br /> * Genotype<br /> * Heterozygote<br /> * Homozygote<br /> * Humans<br /> * Longevity<br /> * Lung Neoplasms<br /> * Middle Aged<br /> * Polymerase Chain Reaction<br /> * Polymorphism, Genetic<br /> * Smoking<br /> <br /> |full-text-url=https://sci-hub.do/10.1016/j.exger.2010.04.007<br /> }}</div>

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