Autor: Stathopoulos, Constantinos

Skocz do pozycji: 1.

Tytuł:: Genomics and the evolution of aminoacyl-tRNA synthesis.
Autorzy:: Ruan, Benfang
Ahel, Ivan
Ambrogelly, Alex
Becker, Hubert
Bunjun, Shipra
Feng, Liang
Tumbula-Hansen, Debra
Ibba, Michael
Korencic, Dragana
Kobayashi, Hiroyuki
Jacquin-Becker, Clarisse
Mejlhede, Nina
Min, Bokkee
Raczniak, Gregory
Rinehart, Jesse
Stathopoulos, Constantinos
Li, Tong
Söll, Dieter
Tematy:: evolution
tRNA
aminoacyl-tRNA
translation
protein synthesis; Pokaż więcej
Wydawca:: Polskie Towarzystwo Biochemiczne
Powiązania:: https://bibliotekanauki.pl/articles/1044116.pdf Link otwiera się w nowym oknie
Opis:: Translation is the process by which ribosomes direct protein synthesis using the genetic information contained in messenger RNA (mRNA). Transfer RNAs (tRNAs) are charged with an amino acid and brought to the ribosome, where they are paired with the corresponding trinucleotide codon in mRNA. The amino acid is attached to the nascent polypeptide and the ribosome moves on to the next codon. Thus, the sequential pairing of codons in mRNA with tRNA anticodons determines the order of amino acids in a protein. It is therefore imperative for accurate translation that tRNAs are only coupled to amino acids corresponding to the RNA anticodon. This is mostly, but not exclusively, achieved by the direct attachment of the appropriate amino acid to the 3'-end of the corresponding tRNA by the aminoacyl-tRNA synthetases. To ensure the accurate translation of genetic information, the aminoacyl-tRNA synthetases must display an extremely high level of substrate specificity. Despite this highly conserved function, recent studies arising from the analysis of whole genomes have shown a significant degree of evolutionary diversity in aminoacyl-tRNA synthesis. For example, non-canonical routes have been identified for the synthesis of Asn-tRNA, Cys-tRNA, Gln-tRNA and Lys-tRNA. Characterization of non-canonical aminoacyl-tRNA synthesis has revealed an unexpected level of evolutionary divergence and has also provided new insights into the possible precursors of contemporary aminoacyl-tRNA synthetases.
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 2.

Tytuł:: Early microvascular coronary endothelial dysfunction precedes pembrolizumab-induced cardiotoxicity. Preventive role of high dose of atorvastatin
Autorzy:: Kostopoulos, Ioannis V.
Chłopicki, Stefan
Choustoulaki, Angeliki
Kwiatkowski, Grzegorz
Briasoulis, Alexandros
Varela, Aimilia
Dimopoulos, Meletios A.
Vorgias, Constantinos E.
Georgoulis, Anastasios
Terpos, Evangelos
Ntanasis-Stathopoulos, Ioannis
Andreadou, Ioanna
Kostomitsopoulos, Nikolaos
Tsitsilonis, Ourania
Gakiopoulou, Harikleia
Davos, Constantinos H.
Efentakis, Panagiotis
Tsekenis, George
Gavriatopoulou, Maria
Opis:: Immune checkpoint inhibitors (ICIs) exhibit remarkable antitumor activity and immune-related cardiotoxicity of unknown pathomechanism. The aim of the study was to investigate the ICI class-dependent cardiotoxicity in vitro and pembrolizumab's (Pem's) cardiotoxicity in vivo, seeking for translational prevention means. Cytotoxicity was investigated in primary cardiomyocytes and splenocytes, incubated with ipilimumab, Pem and avelumab. Pem’s cross-reactivity was assessed by circular dichroism (CD) on biotechnologically produced human and murine PD-1 and in silico. C57BL6/J male mice received IgG4 or Pem for 2 and 5 weeks. Echocardiography, histology, and molecular analyses were performed. Coronary blood flow velocity mapping and cardiac magnetic resonance imaging were conducted at 2 weeks. Human EA.hy926 endothelial cells were incubated with Pem-conditioned media from human mononuclear cells, in presence and absence of statins and viability and molecular signaling were assessed. Atorvastatin (20 mg/kg, daily) was administered in vivo, as prophylaxis. Only Pem exerted immune-related cytotoxicity in vitro. Pem’s cross-reactivity with the murine PD-1 was confirmed by CD and docking. In vivo, Pem initiated coronary endothelial and diastolic dysfunction at 2 weeks and systolic dysfunction at 5 weeks. At 2 weeks, Pem induced ICAM-1 and iNOS expression and intracardiac leukocyte infiltration. At 5 weeks, Pem exacerbated endothelial activation and triggered cardiac inflammation. Pem led to immune-related cytotoxicity in EA.hy926 cells, which was prevented by atorvastatin. Atorvastatin mitigated functional deficits, by inhibiting endothelial dysfunction in vivo. We established for the first time an in vivo model of Pem-induced cardiotoxicity. Coronary endothelial dysfunction precedes Pem-induced cardiotoxicity, whereas atorvastatin emerges as a novel prophylactic therapy.
Dostawca treści:: Repozytorium Uniwersytetu Jagiellońskiego

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