-
Notifications
You must be signed in to change notification settings - Fork 0
/
webpage_literature.bib
162 lines (155 loc) · 13.2 KB
/
webpage_literature.bib
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
81
82
83
84
85
86
87
88
89
90
91
92
93
94
95
96
97
98
99
100
101
102
103
104
105
106
107
108
109
110
111
112
113
114
115
116
117
118
119
120
121
122
123
124
125
126
127
128
129
130
131
132
133
134
135
136
137
138
139
140
141
142
143
144
145
146
147
148
149
150
151
152
153
154
155
156
157
158
159
160
161
162
@Article{Fricke:18,
author = {Fricke, Markus and Gerst, Ruman and Ibrahim, Bashar and Niepmann, Michael and Marz, Manja},
title = {Global importance of {RNA} secondary structures in protein coding sequences.},
journal = {Bioinformatics},
year = {2018},
issn = {1367-4811},
abstract = {The protein-coding sequences of messenger RNAs are the linear template for translation of the gene sequence into protein. Nevertheless, the RNA can also form secondary structures by intramolecular base-pairing. We show that the nucleotide distribution within codons is biased in all taxa of life on a global scale. Thereby, RNA secondary structures that require base-pairing between the position 1 of a codon with the position 1 of an opposing codon (here named RNA secondary structure class c1) are under-represented. We conclude that this bias may result from the co-evolution of codon sequence and mRNA secondary structure, suggesting that RNA secondary structures are generally important in protein coding regions of mRNAs. The above result also implies that codon position 2 has a smaller influence on the amino acid choice than codon position 1.},
country = {England},
doi = {10.1093/bioinformatics/bty678},
issn-linking = {1367-4803},
nlm-id = {9808944},
owner = {NLM},
pii = {5067859},
pmid = {30101307},
pubmodel = {Print-Electronic},
pubstatus = {aheadofprint},
revised = {2018-08-13},
}
@Article{Ibrahim:18,
author = {Ibrahim, Bashar and Arkhipova, Ksenia and Andeweg, Arno C and Posada-C\'{e}spedes, Susana and Enault, Fran\c{c}ois and Gruber, Arthur and Koonin, Eugene V and Kupczok, Anne and Lemey, Philippe and McHardy, Alice C and McMahon, Dino P and Pickett, Brett E and Robertson, David L and Scheuermann, Richard H and Zhernakova, Alexandra and Zwart, Mark P and Sch\"{o}nhuth, Alexander and Dutilh, Bas E and Marz, Manja},
title = {Bioinformatics Meets Virology: The {E}uropean {V}irus {B}ioinformatics {C}enter's Second Annual Meeting.},
journal = {Viruses},
year = {2018},
volume = {10},
month = may,
issn = {1999-4915},
abstract = {The Second Annual Meeting of the European Virus Bioinformatics Center (EVBC), held in Utrecht, Netherlands, focused on computational approaches in virology, with topics including (but not limited to) virus discovery, diagnostics, (meta-)genomics, modeling, epidemiology, molecular structure, evolution, and viral ecology. The goals of the Second Annual Meeting were threefold: (i) to bring together virologists and bioinformaticians from across the academic, industrial, professional, and training sectors to share best practice; (ii) to provide a meaningful and interactive scientific environment to promote discussion and collaboration between students, postdoctoral fellows, and both new and established investigators; (iii) to inspire and suggest new research directions and questions. Approximately 120 researchers from around the world attended the Second Annual Meeting of the EVBC this year, including 15 renowned international speakers. This report presents an overview of new developments and novel research findings that emerged during the meeting.},
country = {Switzerland},
doi = {10.3390/v10050256},
issn-linking = {1999-4915},
issue = {5},
keywords = {bioinformatics; software; virology; viruses},
nlm-id = {101509722},
owner = {NLM},
pii = {E256},
pmc = {PMC5977249},
pmid = {29757994},
pubmodel = {Electronic},
pubstatus = {epublish},
revised = {2018-11-14},
}
@Article{Ibrahim:18a,
author = {Ibrahim, Bashar and McMahon, Dino P and Hufsky, Franziska and Beer, Martin and Deng, Li and Mercier, Philippe Le and Palmarini, Massimo and Thiel, Volker and Marz, Manja},
title = {A new era of virus bioinformatics.},
journal = {Virus Res},
year = {2018},
volume = {251},
pages = {86--90},
month = jun,
issn = {1872-7492},
abstract = {Despite the recognized excellence of virology and bioinformatics, these two communities have interacted surprisingly sporadically, aside from some pioneering work on HIV-1 and influenza. Bringing together the expertise of bioinformaticians and virologists is crucial, since very specific but fundamental computational approaches are required for virus research, particularly in an era of big data. Collaboration between virologists and bioinformaticians is necessary to improve existing analytical tools, cloud-based systems, computational resources, data sharing approaches, new diagnostic tools, and bioinformatic training. Here, we highlight current progress and discuss potential avenues for future developments in this promising era of virus bioinformatics. We end by presenting an overview of current technologies, and by outlining some of the major challenges and advantages that bioinformatics will bring to the field of virology.},
citation-subset = {IM},
completed = {2018-09-21},
country = {Netherlands},
doi = {10.1016/j.virusres.2018.05.009},
issn-linking = {0168-1702},
keywords = {Computational Biology, methods, trends; Virology, methods, trends; Viruses, genetics, growth & development; Bioinformatics; Software; Virology; Viruses},
nlm-id = {8410979},
owner = {NLM},
pii = {S0168-1702(18)30225-9},
pmid = {29751021},
pubmodel = {Print-Electronic},
pubstatus = {ppublish},
revised = {2018-09-21},
}
@Article{Steinbach:18,
author = {Steinbach, D and H{\"o}lzer, M and Marz, M and Gajda, M and Von Rundstedt, F-C and Grimm, M-O},
title = {Analysis of molecular mechanism of progression of non-muscle-invasive bladder cancer ({NMIBC}) by genome-wide exome and {UTR} mutation analysis},
journal = {Eur Urol Suppl},
year = {2018},
volume = {17},
number = {2},
pages = {e1523},
owner = {fhufsky},
publisher = {Elsevier},
}
@Article{Hillmann:18,
author = {Hillmann, Falk and Forbes, Gillian and Novohradsk\'{a}, Silvia and Ferling, Iuliia and Riege, Konstantin and Groth, Marco and Westermann, Martin and Marz, Manja and Spaller, Thomas and Winckler, Thomas and Schaap, Pauline and Gl\"{o}ckner, Gernot},
title = {Multiple Roots of Fruiting Body Formation in Amoebozoa.},
journal = {Genome Biol Evol},
year = {2018},
volume = {10},
pages = {591--606},
month = feb,
issn = {1759-6653},
abstract = {Establishment of multicellularity represents a major transition in eukaryote evolution. A subgroup of Amoebozoa, the dictyosteliids, has evolved a relatively simple aggregative multicellular stage resulting in a fruiting body supported by a stalk. Protosteloid amoeba, which are scattered throughout the amoebozoan tree, differ by producing only one or few single stalked spores. Thus, one obvious difference in the developmental cycle of protosteliids and dictyosteliids seems to be the establishment of multicellularity. To separate spore development from multicellular interactions, we compared the genome and transcriptome of a Protostelium species (Protostelium aurantium var. fungivorum) with those of social and solitary members of the Amoebozoa. During fruiting body formation nearly 4,000 genes, corresponding to specific pathways required for differentiation processes, are upregulated. A comparison with genes involved in the development of dictyosteliids revealed conservation of >500 genes, but most of them are also present in Acanthamoeba castellanii for which fruiting bodies have not been documented. Moreover, expression regulation of those genes differs between P. aurantium and Dictyostelium discoideum. Within Amoebozoa differentiation to fruiting bodies is common, but our current genome analysis suggests that protosteliids and dictyosteliids used different routes to achieve this. Most remarkable is both the large repertoire and diversity between species in genes that mediate environmental sensing and signal processing. This likely reflects an immense adaptability of the single cell stage to varying environmental conditions. We surmise that this signaling repertoire provided sufficient building blocks to accommodate the relatively simple demands for cell-cell communication in the early multicellular forms.},
chemicals = {Protozoan Proteins},
citation-subset = {IM},
completed = {2018-10-15},
country = {England},
doi = {10.1093/gbe/evy011},
issn-linking = {1759-6653},
issue = {2},
keywords = {Amoebozoa, cytology, genetics, growth & development; Cell Communication; Dictyostelium, cytology, genetics, growth & development; Evolution, Molecular; Gene Expression Regulation, Developmental; Phylogeny; Protozoan Proteins, genetics; Transcriptome; Amoebozoa; Dictyostelia; Protostelium; evolution of development; multicellular development; signaling; transcriptome},
nlm-id = {101509707},
owner = {NLM},
pii = {4824916},
pmc = {PMC5804921},
pmid = {29378020},
pubmodel = {Print},
pubstatus = {ppublish},
revised = {2018-11-13},
}
@Article{Hufsky:18,
author = {Hufsky, Franziska and Ibrahim, Bashar and Beer, Martin and Deng, Li and Mercier, Philippe Le and McMahon, Dino P and Palmarini, Massimo and Thiel, Volker and Marz, Manja},
title = {Virologists-Heroes need weapons.},
journal = {PLoS Pathog},
year = {2018},
volume = {14},
pages = {e1006771},
month = feb,
issn = {1553-7374},
__markedentry = {[fhufsky:]},
citation-subset = {IM},
completed = {2018-06-22},
country = {United States},
doi = {10.1371/journal.ppat.1006771},
issn-linking = {1553-7366},
issue = {2},
keywords = {Animals; Biomedical Research, manpower, methods, trends; Computational Biology, manpower, methods, trends; Europe; Humans; Professional Role; Virology, manpower, methods, trends},
nlm-id = {101238921},
owner = {NLM},
pii = {PPATHOGENS-D-17-02282},
pmc = {PMC5805341},
pmid = {29420617},
pubmodel = {Electronic-eCollection},
pubstatus = {epublish},
revised = {2018-11-13},
}
@Article{Graf:18,
author = {Graf, Laura and Dick, Alexej and Sendker, Franziska and Barth, Emanuel and Marz, Manja and Daumke, Oliver and Kochs, Georg},
title = {Effects of allelic variations in the human myxovirus resistance protein {A} on its antiviral activity.},
journal = {J Biol Chem},
year = {2018},
volume = {293},
pages = {3056--3072},
month = mar,
issn = {1083-351X},
__markedentry = {[fhufsky:6]},
abstract = {Only a minority of patients infected with seasonal influenza A viruses exhibit a severe or fatal outcome of infection, but the reasons for this inter-individual variability in influenza susceptibility are unclear. To gain further insights into the molecular mechanisms underlying this variability, we investigated naturally occurring allelic variations of the myxovirus resistance 1 ( ) gene coding for the influenza restriction factor MxA. The interferon-induced dynamin-like GTPase consists of an N-terminal GTPase domain, a bundle signaling element, and a C-terminal stalk responsible for oligomerization and viral target recognition. We used online databases to search for variations in the gene. Deploying approaches, we found that non-synonymous variations in the GTPase domain cause the loss of antiviral and enzymatic activities. Furthermore, we showed that these amino acid substitutions disrupt the interface for GTPase domain dimerization required for the stimulation of GTP hydrolysis. Variations in the stalk were neutral or slightly enhanced or abolished MxA antiviral function. Remarkably, two other stalk variants altered MxA's antiviral specificity. Variations causing the loss of antiviral activity were found only in heterozygous carriers. Interestingly, the inactive stalk variants blocked the antiviral activity of WT MxA in a dominant-negative way, suggesting that heterozygotes are phenotypically MxA-negative. In contrast, the GTPase-deficient variants showed no dominant-negative effect, indicating that heterozygous carriers should remain unaffected. Our results demonstrate that naturally occurring mutations in the human gene can influence MxA function, which may explain individual variations in influenza virus susceptibility in the human population.},
country = {United States},
doi = {10.1074/jbc.M117.812784},
issn-linking = {0021-9258},
issue = {9},
keywords = {Mx proteins; allelic variations; antiviral response; dynamin; genetic polymorphism; influenza virus; innate immunity; interferon},
nlm-id = {2985121R},
owner = {NLM},
pii = {M117.812784},
pmc = {PMC5836113},
pmid = {29330299},
pubmodel = {Print-Electronic},
pubstatus = {ppublish},
revised = {2018-11-13},
}
@Comment{jabref-meta: databaseType:bibtex;}