001     137186
005     20240321220215.0
024 7 _ |a 10.1042/BJ20130788
|2 doi
024 7 _ |a pmid:24059268
|2 pmid
024 7 _ |a 0006-2936
|2 ISSN
024 7 _ |a 0264-6021
|2 ISSN
024 7 _ |a 0306-3275
|2 ISSN
024 7 _ |a 0306-3283
|2 ISSN
024 7 _ |a 1470-8728
|2 ISSN
024 7 _ |a altmetric:1778220
|2 altmetric
037 _ _ |a DZNE-2020-03508
041 _ _ |a English
082 _ _ |a 540
100 1 _ |a Wirth, Alexander
|0 P:(DE-HGF)0
|b 0
245 _ _ |a Dual lipidation of the brain-specific Cdc42 isoform regulates its functional properties.
260 _ _ |a London
|c 2013
|b Portland Press67261
264 _ 1 |3 online
|2 Crossref
|b Portland Press Ltd.
|c 2013-11-22
264 _ 1 |3 print
|2 Crossref
|b Portland Press Ltd.
|c 2013-12-15
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 1586266615_6465
|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 Cdc42 (cell division cycle 42) is a member of the Rho GTPase family which regulates a variety of cellular activities by controlling actin cytoskeleton and gene expression. Cdc42 is expressed in the form of two splice variants. The canonical Cdc42 isoform is prenylated (Cdc42-prenyl), whereas the brainspecific isoform can be palmitoylated (Cdc42-palm). In the present study we have demonstrated palmitoylation of endogenous Cdc42 in rodent and human brains and identified Cys(188) and Cys(189) as acylation sites of Cdc42-palm. Moreover, we have shown that Cys(188) can also be prenylated. Analysis of acylation-deficient mutants revealed that lipidation of Cys(188) is essential for proper membrane binding of Cdc42-palm as well as for Cdc42-mediated regulation of gene transcription and induction of densely packed filopodia in neuroblastoma cells. We also found that Cdc42-prenyl is a dominant splice variant in a wide range of commonly used cell lines as well as in the cerebellum, whereas Cdc42-palm is the main Cdc42 isoform in hippocampus, where it is critically involved in the formation of dendritic filopodia and spines. Replacement of endogenous Cdc42 by its acylation-deficient mutants revealed the importance of Cdc42-palm lipidation for its morphogenic and synaptogenic effects in neurons. These findings demonstrate that dual lipidation of Cdc42-palm represents an important regulator of morphogenic signalling in hippocampal neurons.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
|0 G:(DE-HGF)POF3-342
|c POF3-342
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Cdc42 protein, mouse
|2 NLM Chemicals
650 _ 7 |a Isoenzymes
|2 NLM Chemicals
650 _ 7 |a cdc42 GTP-Binding Protein
|0 EC 3.6.5.2
|2 NLM Chemicals
650 _ 7 |a Cysteine
|0 K848JZ4886
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Cell Line, Tumor
|2 MeSH
650 _ 2 |a Cerebellum: cytology
|2 MeSH
650 _ 2 |a Cerebellum: metabolism
|2 MeSH
650 _ 2 |a Cysteine: genetics
|2 MeSH
650 _ 2 |a Cysteine: metabolism
|2 MeSH
650 _ 2 |a Dendrites: genetics
|2 MeSH
650 _ 2 |a Dendrites: metabolism
|2 MeSH
650 _ 2 |a Hippocampus: cytology
|2 MeSH
650 _ 2 |a Hippocampus: metabolism
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Isoenzymes: genetics
|2 MeSH
650 _ 2 |a Isoenzymes: metabolism
|2 MeSH
650 _ 2 |a Lipoylation: physiology
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Organ Specificity: physiology
|2 MeSH
650 _ 2 |a Protein Prenylation: physiology
|2 MeSH
650 _ 2 |a Pseudopodia: genetics
|2 MeSH
650 _ 2 |a Pseudopodia: metabolism
|2 MeSH
650 _ 2 |a Transcription, Genetic: physiology
|2 MeSH
650 _ 2 |a cdc42 GTP-Binding Protein: genetics
|2 MeSH
650 _ 2 |a cdc42 GTP-Binding Protein: metabolism
|2 MeSH
700 1 _ |a Chen-Wacker, Chen
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Wu, Yao-Wen
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Gorinski, Nataliya
|0 P:(DE-HGF)0
|b 3
700 1 _ |a Filippov, Mikhail A
|0 P:(DE-2719)2810721
|b 4
|u dzne
700 1 _ |a Pandey, Ghanshyam
|0 P:(DE-HGF)0
|b 5
700 1 _ |a Ponimaskin, Evgeni
|0 P:(DE-HGF)0
|b 6
|e Corresponding author
773 1 8 |a 10.1042/bj20130788
|b : Portland Press Ltd., 2013-11-22
|n 3
|p 311-322
|3 journal-article
|2 Crossref
|t Biochemical Journal
|v 456
|y 2013
|x 0264-6021
773 _ _ |a 10.1042/BJ20130788
|g Vol. 456, no. 3, p. 311 - 322
|0 PERI:(DE-600)1473095-9
|n 3
|q 456:3<311 - 322
|p 311-322
|t Biochemical journal
|v 456
|y 2013
|x 0264-6021
909 C O |o oai:pub.dzne.de:137186
|p VDB
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 4
|6 P:(DE-2719)2810721
913 1 _ |a DE-HGF
|b Forschungsbereich Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-342
|2 G:(DE-HGF)POF3-300
|v Disease Mechanisms and Model Systems
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914 1 _ |y 2013
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LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21