tRNA Metabolism and Lung Cancer: Beyond Translation
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Lung cancer, one of the most malignant tumors, has extremely high morbidity and mortality, posing a serious threat to global health. It is an urgent need to fully understand the pathogenesis of lung cancer and provide new ideas for its treatment. Interestingly, accumulating evidence has identified that transfer RNAs (tRNAs) and tRNA metabolism-associated enzymes not only participate in the protein translation but also play an important role in the occurrence and development of lung cancer. In this review, we summarize the different aspects of tRNA metabolism in lung cancer, such as tRNA transcription and mutation, tRNA molecules and derivatives, tRNA-modifying enzymes, and aminoacyl-tRNA synthetases (ARSs), aiming at a better understanding of the pathogenesis of lung cancer and providing new therapeutic strategies for it.Keywords:
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Transcription
The tRNA Thr 2 isoacceptor of E. coli has a G‐A mismatch at positions 27–43. When the anticodon of this tRNA was converted to an amber anticodon (CUA), this tRNA showed suppressor activity in E. coli . Moreover, introduction of the base pair (G‐C or U‐A) at positions 27–43 of this suppressor tRNA reduced its suppressor activity. These results indicate that the G27‐A43 mismatch is necessary for full function of tRNA Thr 2 .
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The characteristic of the dynamic time is coincidence with its internal pathogenesis.The pathogenesis,however,has different levels.The basic pathogenesis is located at the highest level.The basic pathogenesis guides the specific pathogenesis,and the later is subordinated to the basic one.From the study of the basic pathogenesis we can conclude that therapy in group combinating with individual therapy is the essence of differentiated treatment
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The association between Trp-tRNA and Pro-tRNA; which have complementary anticodon sequences, has been used as a probe of anticodon conformation. It is unaffected, however, by the base change in the D-stem present in UGA-suppressor Trp—tRNA. This does not support the hypothesis that UGA suppression depends upon a conformational change induced in the anticodon. The stable denatured form of wild-type Trp-tRNA no longer interacts with Pro-tRNA ; the structure of the anticodon region must therefore be quite different in the denatured form.
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We have constructed an opal suppressor system in Escherichia coli to complement an existing amber suppressor system to study the structural basis of tRNA acceptor identity, particularly the role of middle anticodon nucleotide at position 35. The opal suppressor tRNA contains a UCA anticodon and the mRNA of the suppressed protein (which is easily purified and sequenced) contains a UGA nonsense triplet. Opal suppressor tRNAs of two tRNA(Arg) isoacceptor sequences each gave arginine in the suppressed protein, while the corresponding amber suppressors with U35 in their CUA anticodons each gave arginine plus a second amino acid in the suppressed protein. Since C35 but not U35 is present in the anticodon of wild-type tRNA(Arg) molecules, while the first anticodon position contains either C34 or U34, these results establish that C35 contributes to tRNA(Arg) acceptor identity. Initial characterizations of opal suppressor tRNA(Arg) mutants by suppression efficiency measurements suggest that the fourth nucleotide from the 3' end of tRNA(Arg) (A73 or G73 in different isoacceptors) also contributes to tRNA(Arg) acceptor identity. Wild-type and mutant versions of opal and amber tRNA(Lys) suppressors were examined, revealing that U35 and A73 are important determinants of tRNA(Lys) acceptor identity. Several possibilities are discussed for the general significance of having tRNA acceptor identity in the same positions in different tRNA acceptor types, as exemplified by positions 35 and 73 in tRNA(Arg) and tRNA(Lys).
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The pathogenesis in idiopathic inflammatory myopathies(IIM) remain undefined so far.Previous studies on IIM focused on immunopathogenesis and suggested that IIM was autoimmune.Studies on nonimmune pathogenesis are insufficient.This review summarizes the update on pathogenesis in IIM, including immune and nonimmune processes.
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To review the research progress of heterotopic ossification (HO) pathogenesis.Recent articles about HO including the risk factors and pathogenesis were reviewed and comprehensively analyzed.The pathogenesis of HO is not completely understood, but the extracellular factors, signaling pathways, and transcription factors in the pathogenesis of HO are understood deeply, such as bone morphogenic protein, Smad signaling, and core binding factor alpha1/runt-related transcription factor 2, which are probably involved in HO. Furthermore, some related microRNAs are also probably involved in HO.The pathogenesis of HO should be further investigated so as to lay a foundation for preventing and treating HO.
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Abstract We have used the temperature-jump relaxation technique to determine the kinetic and thermodynamic parameters for the association between the following tRNAs pairs having complementary anticodons: tRNA(Ser) with tRNA(Gly), tRNA(Cys) with tRNA(Ala) and tRNA(Trp) with tRNA(Pro). The anticodon sequence of E.coli tRNA(Ser), GGA, is complementary to the U*CC anticodon of E.coli tRNA(Gly(2)) (where U* is a still unknown modified uridine base) and A37 is not modified in none of these two tRNAs. E.coli tRNA(Ala) has a VGC anticodon (V is 5-oxyacetic acid uridine) while tRNA(Cys) has the complementary GCA anticodon with a modified adenine on the 3′ side, namely 2-methylthio N6-isopentenyl adenine (mS2i6A37) in E.Coli tRNA(Cys) and N6-isopentenyl adenine (i6A37) in yeast tRNA(Cys). The brewer yeast tRNA(Trp) (anticodon CmCA) differs from the wild type E.coli tRNA(Trp) (anticodon CCA) in several positions of the nucleotide sequence. Nevertheless, in the anticodon loop, only two interesting differences are present: A37 is not modified while C34 at the first anticodon position is modified into a ribose 2′—O methyl derivative (Cm). The corresponding complementary tRNA is E.coli tRNA(Pro) with the VGG anticodon. Our results indicate a dominant effect of the nature and sequence of the anticodon bases and their nearest neighbor in the anticodon loop (particularly at position 37 on the 3′ side); no detectable influence of modifications in the other tRNA stems has been detected. We found a strong stabilizing effect of the methylthio group on i6A37 as compared to isopentenyl modification of the same residue. We have not been able so far to assess the effect of isopentenyl modification alone in comparison to unmodified A37. The results obtained with the complex yeast tRNA(Trp) -E.coli tRNA(Pro) also suggest that a modification of C34 to Cm34 does not significantly increase the stability of tRNA(Trp) association with its complementary anticodon in tRNA(Pro). The observations are discussed in the light of inter- and intra-strand stacking interactions among the anticodon triplets and with the purine base adjacent to them, and of possible biological implications.
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Objective:To analyze the pathogenesis and correlative factors of acute upper gastrointestinal hemorrhage.Methods:90 cases with acute upper gastrointestinal hemorrhage from Jan 2010 to Jun 2012 in our hospital were selected as the research objectives.The pathogenesis,predisposition and correlative factors were analyzed using the statistical method.Results:HG,DU,GU were the main pathogenesis of acute upper gastrointestinal hemorrhage.Different pathogeneses had different predispositions(P0.01).Pathogenesis distribution in Youth group,middle-aged group,and older age-group were different(P0.01).Pathogenesis distribute in male and female had no significant difference(P0.05).Conclusions:There are lots of Pathogeneses of acute upper gastrointestinal hemorrhage,and pathogenesis distribution in different age classes is different.
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Hypertension has complicated pathogenesis.Because of the complexity,in this article the hypertension pathogenesis was divided into several different levels to discuss,which were basic pathogenesis,syndrome pathogenesis,symptom manifestation pathogenesis,disease pathogenesis and micro pathogenesis.The relationship between the above levels and the theoretic and clinical values of each level were analyzed.The significance of syndrome pathogenesis in the study on hypertension pathogenesis was emphasized.
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