Home > Publications database > Medulloblastoma-associated DDX3 variant selectively alters the translational response to stress. > print

001     130276
005     20240228143421.0
024 7 _ |a 10.18632/oncotarget.8612
|2 doi
024 7 _ |a pmid:27058758
|2 pmid
024 7 _ |a pmc:PMC5053718
|2 pmc
024 7 _ |a altmetric:6575508
|2 altmetric
037 _ _ |a DKFZ-2017-05355
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Oh, Sekyung
|b 0
245 _ _ |a Medulloblastoma-associated DDX3 variant selectively alters the translational response to stress.
260 _ _ |a [S.l.]
|c 2016
|b Impact Journals LLC
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1522134988_11125
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a DDX3X encodes a DEAD-box family RNA helicase (DDX3) commonly mutated in medulloblastoma, a highly aggressive cerebellar tumor affecting both children and adults. Despite being implicated in several facets of RNA metabolism, the nature and scope of DDX3s interactions with RNA remain unclear. Here, we show DDX3 collaborates extensively with the translation initiation machinery through direct binding to 5UTRs of nearly all coding RNAs, specific sites on the 18S rRNA, and multiple components of the translation initiation complex. Impairment of translation initiation is also evident in primary medulloblastomas harboring mutations in DDX3X, further highlighting DDX3s role in this process. Arsenite-induced stress shifts DDX3 binding from the 5UTR into the coding region of mRNAs concomitant with a general reduction of translation, and both the shift of DDX3 on mRNA and decreased translation are blunted by expression of a catalytically-impaired, medulloblastoma-associated DDX3R534H variant. Furthermore, despite the global repression of translation induced by arsenite, translation is preserved on select genes involved in chromatin organization in DDX3R534H-expressing cells. Thus, DDX3 interacts extensively with RNA and ribosomal machinery to help remodel the translation landscape in response to stress, while cancer-related DDX3 variants adapt this response to selectively preserve translation.
536 _ _ |a 312 - Functional and structural genomics (POF3-312)
|0 G:(DE-HGF)POF3-312
|c POF3-312
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
700 1 _ |a Flynn, Ryan A
|b 1
700 1 _ |a Floor, Stephen N
|b 2
700 1 _ |a Purzner, James
|b 3
700 1 _ |a Martin, Lance
|b 4
700 1 _ |a Do, Brian T
|b 5
700 1 _ |a Schubert, Simone
|b 6
700 1 _ |a Vaka, Dedeepya
|b 7
700 1 _ |a Morrissy, Sorana
|b 8
700 1 _ |a Li, Yisu
|b 9
700 1 _ |a Kool, Marcel
|0 P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8
|b 10
|u dkfz
700 1 _ |a Hovestadt, Volker
|0 P:(DE-He78)744146d3b5a3df1e0ac555e5bf1ee5cc
|b 11
|u dkfz
700 1 _ |a Jones, David
|0 P:(DE-He78)551bb92841f634070997aa168d818492
|b 12
|u dkfz
700 1 _ |a Northcott, Paul A
|0 P:(DE-HGF)0
|b 13
700 1 _ |a Risch, Thomas
|b 14
700 1 _ |a Warnatz, Hans-Jörg
|b 15
700 1 _ |a Yaspo, Marie-Laure
|b 16
700 1 _ |a Adams, Christopher M
|b 17
700 1 _ |a Leib, Ryan D
|b 18
700 1 _ |a Breese, Marcus
|b 19
700 1 _ |a Marra, Marco A
|b 20
700 1 _ |a Malkin, David
|b 21
700 1 _ |a Lichter, Peter
|0 P:(DE-He78)e13b4363c5fe858044ef8a39c02c870c
|b 22
|u dkfz
700 1 _ |a Doudna, Jennifer A
|b 23
700 1 _ |a Pfister, Stefan
|0 P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9
|b 24
|u dkfz
700 1 _ |a Taylor, Michael D
|b 25
700 1 _ |a Chang, Howard Y
|b 26
700 1 _ |a Cho, Yoon-Jae
|b 27
773 _ _ |a 10.18632/oncotarget.8612
|g Vol. 7, no. 19, p. 28169 - 28182
|0 PERI:(DE-600)2560162-3
|n 19
|p 28169 - 28182
|t OncoTarget
|v 7
|y 2016
|x 1949-2553
909 C O |o oai:inrepo02.dkfz.de:130276
|p VDB
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 10
|6 P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 11
|6 P:(DE-He78)744146d3b5a3df1e0ac555e5bf1ee5cc
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 12
|6 P:(DE-He78)551bb92841f634070997aa168d818492
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 13
|6 P:(DE-HGF)0
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 22
|6 P:(DE-He78)e13b4363c5fe858044ef8a39c02c870c
910 1 _ |a Deutsches Krebsforschungszentrum
|0 I:(DE-588b)2036810-0
|k DKFZ
|b 24
|6 P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9
913 1 _ |a DE-HGF
|l Krebsforschung
|1 G:(DE-HGF)POF3-310
|0 G:(DE-HGF)POF3-312
|2 G:(DE-HGF)POF3-300
|v Functional and structural genomics
|x 0
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF3
|b Gesundheit
914 1 _ |y 2016
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b ONCOTARGET : 2015
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0310
|2 StatID
|b NCBI Molecular Biology Database
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Thomson Reuters Master Journal List
915 _ _ |a WoS
|0 StatID:(DE-HGF)0111
|2 StatID
|b Science Citation Index Expanded
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b ONCOTARGET : 2015
920 1 _ |0 I:(DE-He78)B062-20160331
|k B062
|l Pädiatrische Neuroonkologie
|x 0
920 1 _ |0 I:(DE-He78)B060-20160331
|k B060
|l Molekulare Genetik
|x 1
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-He78)B062-20160331
980 _ _ |a I:(DE-He78)B060-20160331
980 _ _ |a UNRESTRICTED

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21