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Diphthamide modification on eukaryotic elongation factor 2 is needed to assure fidelity of mRNA translation and mouse development

Liu, S. ; Bachran, C. ; Gupta, P. ; Miller-Randolph, S. ; Wang, H. ; Crown, D. ; Zhang, Y. ; Wein, A. N. ; Singh, R. ; Fattah, R. ; Leppla, S. H.

Proceedings of the National Academy of Sciences, 08/21/2012, Vol.109(34), pp.13817-13822 [Tạp chí có phản biện]

ISSN: 0027-8424 ; E-ISSN: 1091-6490 ; DOI: http://dx.doi.org/10.1073/pnas.1206933109

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  • Nhan đề:
    Diphthamide modification on eukaryotic elongation factor 2 is needed to assure fidelity of mRNA translation and mouse development
  • Tác giả: Liu, S. ; Bachran, C. ; Gupta, P. ; Miller-Randolph, S. ; Wang, H. ; Crown, D. ; Zhang, Y. ; Wein, A. N. ; Singh, R. ; Fattah, R. ; Leppla, S. H.
  • Chủ đề: Microrna -- Physiological Aspects ; Translocations (Genetics) -- Research ; Embryonic Development -- Physiological Aspects ; Embryonic Development -- Genetic Aspects ; Amino Acids -- Physiological Aspects ; Amino Acids -- Genetic Aspects
  • Là 1 phần của: Proceedings of the National Academy of Sciences, 08/21/2012, Vol.109(34), pp.13817-13822
  • Mô tả: To study the role of the diphthamide modification on eukaryotic elongation factor 2 (eEF2), we generated an eEF2 [Gly.sup.717]Arg mutant mouse, in which the first step of diphthamide biosynthesis is prevented. Interestingly, the [Gly.sup.717]-to-Arg mutation partially compensates the eEF2 functional loss resulting from diphthamide deficiency, possibly because the added +1 charge compensates for the loss of the +1 charge on diphthamide. Therefore, in contrast to mouse embryonic fibroblasts (MEFs) from [OVCA1.sup.-/-] mice, [eEF2.sup.G717R/G717R] MEFs retain full activity in polypeptide elongation and have normal growth rates. Furthermore, [eEF2.sup.G717R/G717R] mice showed milder phenotypes than [OVCA1.sup.-/-] mice (which are 100% embryonic lethal) and a small fraction survived to adulthood without obvious abnormalities. Moreover, [eEF2.sup.G717R/G717R]/[OvCA1.sup.-l-] double mutant mice displayed the milder phenotypes of the [eEF2.sup.G717R/G717R] mice, suggesting that the embryonic lethality of [OVCA1.sup.-/-] mice is due to diphthamide deficiency. We confirmed that the diphthamide modification is essential for eEF2 to prevent -1 frameshifting during translation and show that the [Gly.sup.717]-to-Arg mutation cannot rescue this defect. www.pnas.org/cgi/doi/10.1073/pnas.1206933109
  • Ngôn ngữ: English
  • Số nhận dạng: ISSN: 0027-8424 ; E-ISSN: 1091-6490 ; DOI: http://dx.doi.org/10.1073/pnas.1206933109

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