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1 signaling pathway is affected by deletion of diphthamide.
2 PH4, and DPH5 generated viable cells without diphthamide.
3 cidation of the full biosynthesis pathway of diphthamide.
4 compensates for the loss of the +1 charge on diphthamide.
5 through CRISPR/Cas9-mediated knockout of the diphthamide 1 (DPH1) gene, which enable both robust viru
6 on of codon-anticodon interactions involving diphthamide(1) and the hypermodified nucleoside wybutosi
7 hat loss of the intracellular target for DT, diphthamide, a conservative modification of histidine 71
8                   The structure explains how diphthamide, a eukaryotic and archaeal specific post-tra
9                                              Diphthamide, a modification found only on translation el
10                                              Diphthamide, a posttranslational modification of transla
11                The physiological function of diphthamide and the basis of its ubiquity remain a myste
12 ive studies into the potential regulation of diphthamide, and importantly, its ill-defined biological
13 al modification: the conversion of His699 to diphthamide at the tip of domain IV, the region proposed
14 ibosylation of a modified histidine residue, diphthamide, at His715, which blocks protein translation
15                                          Its diphthamide-bearing tip at domain IV separates the tRNA-
16 ient with compound heterozygous mutations in Diphthamide Biosynthesis 1 (DPH1) and impaired eEF2 diph
17 a type III J-protein playing a vital role in diphthamide biosynthesis and normal development.
18 vel of DPH4 mRNA and protein, which prevents diphthamide biosynthesis and renders EF2 refractory to H
19  a novel gene family that may be involved in diphthamide biosynthesis in humans.
20 ical evidence showing that the first step of diphthamide biosynthesis in the archaeon Pyrococcus hori
21 imer and is sufficient for the first step of diphthamide biosynthesis in vitro.
22                                              Diphthamide biosynthesis is carried out by five highly c
23 Arg mutant mouse, in which the first step of diphthamide biosynthesis is prevented.
24 mplication of this unexpected finding on the diphthamide biosynthesis pathway is discussed.
25 The evolutionary conservation of the complex diphthamide biosynthesis pathway throughout eukaryotes i
26 h7 for the first time and provides a revised diphthamide biosynthesis pathway.
27  catalyzing a previously unknown step in the diphthamide biosynthesis pathway.
28 verse number of species, including the yeast diphthamide biosynthesis protein-2, dph2, which suggeste
29             Nonetheless, the conservation of diphthamide biosynthesis together with syndromes (i.e. r
30 hree decades ago, in vitro reconstitution of diphthamide biosynthesis using purified proteins has not
31 ne in yeast is required for the last step of diphthamide biosynthesis, as the deletion of YBR246W lea
32              In addition to having a role in diphthamide biosynthesis, Dph3 is also involved in modul
33 ty of yeast to zymocin, is also required for diphthamide biosynthesis, implicating DESR1/KTI11 in mul
34 Interestingly, TORC1 signaling also promotes diphthamide biosynthesis, suggesting that diphthamide fo
35 e (SAM) enzyme involved in the first step of diphthamide biosynthesis.
36 three of the proteins involved in eukaryotic diphthamide biosynthesis.
37  diphthamide synthetase for the last step of diphthamide biosynthesis.
38 for important metabolic reactions, including diphthamide biosynthesis.
39 ncluding the noncanonical radical-SAM enzyme diphthamide biosynthetic enzyme Dph1-Dph2, require at le
40 sing agent that, through ADP ribosylation of diphthamide, causes irreversible inactivation of EF2 and
41                                              Diphthamide deficiency in yeast suppresses the translati
42 ates the eEF2 functional loss resulting from diphthamide deficiency, possibly because the added +1 ch
43 and to address the biological consequence of diphthamide deficiency.
44 yonic lethality of OVCA1(-/-) mice is due to diphthamide deficiency.
45 hthamide is evolutionarily conserved and why diphthamide deletion can cause severe developmental defe
46 yotes, exactly what proteins are affected by diphthamide deletion is not clear in cells.
47 gment of cholix toxin was characterized as a diphthamide dependent ADP-ribosyltransferase.
48 es diphthamide biosynthesis, suggesting that diphthamide forms a positive feedback loop to promote tr
49   However, recent progress in dissecting the diphthamide gene network (DPH1-DPH7) from the budding ye
50 ed eukaryotic posttranslational modification diphthamide in eEF2 and tRNA modifications in supporting
51              This finding suggests a role of diphthamide in modulating NF-kappaB, death receptor, or
52 throughout eukaryotes implies a key role for diphthamide in normal cellular physiology.
53                  Surprisingly, cells without diphthamide (independent of which the DPH gene compromis
54         The proposed biosynthesis pathway of diphthamide involves three steps.
55                                              Diphthamide is a conserved modification in archaeal and
56                                              Diphthamide is a modified histidine residue unique for e
57                                     Although diphthamide is conserved among all eukaryotes, exactly w
58   Our results provide an explanation for why diphthamide is evolutionarily conserved and why diphtham
59  and precisely why cells need EF2 to contain diphthamide is hardly understood.
60 learly emphasizes a pathobiological role for diphthamide, its physiological function is unclear, and
61 enzyme in diphthamide synthesis, resulted in diphthamide loss.
62       These mutant strains and those lacking diphthamide modification enzymes showed increased -1 fra
63                        We confirmed that the diphthamide modification is essential for eEF2 to preven
64 ent protein synthesis in eukaryotes requires diphthamide modification of translation elongation facto
65 normal, whereas dph3-/- mice, which lack the diphthamide modification on eEF-2, are embryonic lethal.
66                     To study the role of the diphthamide modification on eukaryotic elongation factor
67                                     Although diphthamide modification was discovered three decades ag
68 tion of proteins, establishes a role for the diphthamide modification, and provides evidence of the a
69 mide Biosynthesis 1 (DPH1) and impaired eEF2 diphthamide modification, we observe multiple defects in
70 ession and NC defects, which is regulated by diphthamide modification.
71 e inactivation still contained predominantly diphthamide-modified eEF2 and were as sensitive to PE an
72 s that cannot make it strongly suggests that diphthamide-modified EF2 occupies an important and trans
73  S(N)1 type mechanism in which attack of the diphthamide nucleophile lags behind departure of the nic
74                                          The diphthamide on human eukaryotic translation elongation f
75 t hydrolyze ADP-ribose-arginine, -cysteine, -diphthamide, or -asparagine bonds.
76               Expression of DPH1, encoding a diphthamide pathway enzyme, was reduced by DNA CpG methy
77 n, furin, KDEL receptor 2, or members of the diphthamide pathway, protected cells.
78                                      Loss of diphthamide prevented ADP ribosylation of eEF2, rendered
79                      In consequence, loss of diphthamide rendered cells hypersensitive toward TNF-med
80  eukaryotic translation elongation factor 2, diphthamide represents one of the most intriguing post-t
81 (R)) of eEF2 by bacterial toxins on a unique diphthamide residue inhibits its translocation activity,
82  toxin catalyzes the ADP ribosylation of the diphthamide residue of eukaryotic elongation factor 2 (e
83 duce cholix, a potent protein toxin that has diphthamide-specific ADP-ribosyltransferase activity aga
84 mpact of complete or partial inactivation on diphthamide synthesis and toxin sensitivity, and to addr
85 opy number reduction does not affect overall diphthamide synthesis and toxin sensitivity.
86 ed DT production in the bacteria, as well as diphthamide synthesis and ZAKalpha/p38-driven NLRP1 phos
87 way and the biochemical players required for diphthamide synthesis but also are likely to foster inno
88                              We analyzed the diphthamide synthesis genes and found that the WDR85 gen
89 mechanisms required to initiate and complete diphthamide synthesis on EF2.
90 ells frequently acquired deficiencies in the diphthamide synthesis pathway, impairing tagraxofusp's a
91                 Of the proteins required for diphthamide synthesis, Dph3 is the smallest, containing
92 )-containing proteins, resulting in impaired diphthamide synthesis, purine metabolism, nucleotide exc
93 n of the DPH1 gene, encoding a key enzyme in diphthamide synthesis, resulted in diphthamide loss.
94 t amidation step, with Dph6 being the actual diphthamide synthetase catalyzing the ATP-dependent amid
95   We found that yeast protein YLR143W is the diphthamide synthetase catalyzing the last amidation ste
96  we identified the previously unknown enzyme diphthamide synthetase for the last step of diphthamide
97                                              Diphthamide synthetase is evolutionarily conserved in eu
98 s region is post-translationally modified to diphthamide, the target for Corynebacterium diphtheriae
99                                              Diphthamide, the target of diphtheria toxin, is a post-t
100                                              Diphthamide, the target of diphtheria toxin, is a unique
101                                              Diphthamide, the target of diphtheria toxin, is a unique
102  elongation factor-2 at His(715) that yields diphthamide, the target site for ADP ribosylation by DT
103                          The biosynthesis of diphthamide was proposed to involve three steps, with th
104                          The biosynthesis of diphthamide was proposed to involve three steps.
105                          The biosynthesis of diphthamide was proposed to occur in three steps requiri
106  and to begin to investigate the function of diphthamide, we generated dph3 knockout mice and showed
107 tant elements of the biosynthetic pathway of diphthamide, which are required for the cytotoxic effect
108 lationally modified histidine residue called diphthamide, which is the target of diphtheria toxin.
109 ationally modified histidine residue, termed diphthamide, which serves as the only target for diphthe
110 in the mutant cells revealed a novel form of diphthamide with an additional methyl group that prevent

 
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