001     45390
005     20200402205930.0
024 7 _ |2 pmid
|a pmid:15817164
024 7 _ |2 DOI
|a 10.1016/j.yexcr.2005.01.012
024 7 _ |2 WOS
|a WOS:000228409100016
037 _ _ |a PreJuSER-45390
041 _ _ |a eng
082 _ _ |a 570
084 _ _ |2 WoS
|a Oncology
084 _ _ |2 WoS
|a Cell Biology
100 1 _ |a Vetterkind, S.
|b 0
|0 P:(DE-HGF)0
245 _ _ |a Binding of Par-4 to the actin cytoskeleton is essential for Par-4/Dlk-mediated apoptosis
260 _ _ |a Orlando, Fla.
|b Academic Press
|c 2005
300 _ _ |a 392 - 408
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|0 0
|2 EndNote
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a article
|2 DRIVER
440 _ 0 |a Experimental Cell Research
|x 0014-4827
|0 13781
|v 305
500 _ _ |a Record converted from VDB: 12.11.2012
520 _ _ |a Prostate apoptosis response-4 (Par-4) is a 38-kDa protein originally identified as a gene product upregulated in prostate cancer cells undergoing apoptosis. Cell death mediated by Par-4 and its interaction partner DAP like kinase (Dlk) is characterized by dramatic changes of the cytoskeleton. To uncover the role of the cytoskeleton in Par-4/Dlk-mediated apoptosis, we analyzed Par-4 for a direct association with cytoskeletal structures. Confocal fluorescence microscopy revealed that endogenous Par-4 is specifically associated with stress fibers in rat fibroblasts. In vitro cosedimentation analyses and in vivo FRET analyses showed that Par-4 directly binds to F-actin. Actin binding is mediated by the N-terminal 266 amino acids, but does not require the C-terminal region of Par-4 containing the leucine zipper and the death domain. Furthermore, the interaction of Par-4 with actin filaments leads to the formation of actin bundles in vitro and in vivo. In rat fibroblasts, this microfilament association is essential for the pro-apoptotic function of Par-4, since both disruption of the actin cytoskeleton by cytochalasin D treatment and overexpression of Par-4 constructs impaired in actin binding result in a significant decrease of apoptosis induction by Par-4 and Dlk. We propose a model, in which Par-4 recruits Dlk to stress fibers, leading to enhanced phosphorylation of the regulatory light chain of myosin II (MLC) and to the induction of apoptosis.
536 _ _ |a Neurowissenschaften
|c L01
|2 G:(DE-HGF)
|0 G:(DE-Juel1)FUEK255
|x 0
588 _ _ |a Dataset connected to Web of Science, Pubmed
650 _ 2 |2 MeSH
|a Actin Cytoskeleton: chemistry
650 _ 2 |2 MeSH
|a Actin Cytoskeleton: metabolism
650 _ 2 |2 MeSH
|a Actins: analysis
650 _ 2 |2 MeSH
|a Actins: metabolism
650 _ 2 |2 MeSH
|a Animals
650 _ 2 |2 MeSH
|a Apoptosis: physiology
650 _ 2 |2 MeSH
|a Apoptosis Regulatory Proteins
650 _ 2 |2 MeSH
|a Calcium-Calmodulin-Dependent Protein Kinases
650 _ 2 |2 MeSH
|a Cardiac Myosins: metabolism
650 _ 2 |2 MeSH
|a Cell Line, Tumor
650 _ 2 |2 MeSH
|a Humans
650 _ 2 |2 MeSH
|a Intracellular Signaling Peptides and Proteins: analysis
650 _ 2 |2 MeSH
|a Intracellular Signaling Peptides and Proteins: genetics
650 _ 2 |2 MeSH
|a Intracellular Signaling Peptides and Proteins: metabolism
650 _ 2 |2 MeSH
|a MAP Kinase Kinase Kinases
650 _ 2 |2 MeSH
|a Male
650 _ 2 |2 MeSH
|a Mice
650 _ 2 |2 MeSH
|a Mutation: genetics
650 _ 2 |2 MeSH
|a Myosin Light Chains: metabolism
650 _ 2 |2 MeSH
|a Phosphorylation
650 _ 2 |2 MeSH
|a Protein-Serine-Threonine Kinases: metabolism
650 _ 2 |2 MeSH
|a Rats
650 _ 2 |2 MeSH
|a Up-Regulation
650 _ 7 |0 0
|2 NLM Chemicals
|a Actins
650 _ 7 |0 0
|2 NLM Chemicals
|a Apoptosis Regulatory Proteins
650 _ 7 |0 0
|2 NLM Chemicals
|a Intracellular Signaling Peptides and Proteins
650 _ 7 |0 0
|2 NLM Chemicals
|a Myosin Light Chains
650 _ 7 |0 0
|2 NLM Chemicals
|a myosin light chain 2
650 _ 7 |0 0
|2 NLM Chemicals
|a prostate apoptosis response-4 protein
650 _ 7 |0 EC 2.7.11.1
|2 NLM Chemicals
|a Protein-Serine-Threonine Kinases
650 _ 7 |0 EC 2.7.11.1
|2 NLM Chemicals
|a death-associated protein kinase
650 _ 7 |0 EC 2.7.11.17
|2 NLM Chemicals
|a Calcium-Calmodulin-Dependent Protein Kinases
650 _ 7 |0 EC 2.7.11.25
|2 NLM Chemicals
|a MAP Kinase Kinase Kinases
650 _ 7 |0 EC 2.7.11.25
|2 NLM Chemicals
|a mitogen-activated protein kinase kinase kinase 12
650 _ 7 |0 EC 3.6.1.-
|2 NLM Chemicals
|a Cardiac Myosins
650 _ 7 |a J
|2 WoSType
653 2 0 |2 Author
|a actin
653 2 0 |2 Author
|a cytoskeleton
653 2 0 |2 Author
|a Par-4
653 2 0 |2 Author
|a Dlk
653 2 0 |2 Author
|a apoptosis
700 1 _ |a Illenberger, S.
|b 1
|0 P:(DE-HGF)0
700 1 _ |a Kubicek, J.
|b 2
|u FZJ
|0 P:(DE-Juel1)VDB10481
700 1 _ |a Boosen, M.
|b 3
|0 P:(DE-HGF)0
700 1 _ |a Appel, S.
|b 4
|0 P:(DE-HGF)0
700 1 _ |a Naim, H. Y.
|b 5
|0 P:(DE-HGF)0
700 1 _ |a Scheidtmann, K.-H.
|b 6
|0 P:(DE-HGF)0
700 1 _ |a Preuss, U.
|b 7
|0 P:(DE-HGF)0
773 _ _ |a 10.1016/j.yexcr.2005.01.012
|g Vol. 305, p. 392 - 408
|p 392 - 408
|q 305<392 - 408
|0 PERI:(DE-600)1466780-0
|t Experimental cell research
|v 305
|y 2005
|x 0014-4827
856 7 _ |u http://dx.doi.org/10.1016/j.yexcr.2005.01.012
909 C O |o oai:juser.fz-juelich.de:45390
|p VDB
913 1 _ |k L01
|v Neurowissenschaften
|l Funktion und Dysfunktion des Nervensystems
|b Leben
|0 G:(DE-Juel1)FUEK255
|x 0
914 1 _ |y 2005
915 _ _ |0 StatID:(DE-HGF)0010
|a JCR/ISI refereed
920 1 _ |k IBI-2
|l Biologische Strukturforschung
|d 31.12.2006
|g IBI
|0 I:(DE-Juel1)VDB58
|x 0
970 _ _ |a VDB:(DE-Juel1)68947
980 _ _ |a VDB
980 _ _ |a ConvertedRecord
980 _ _ |a journal
980 _ _ |a I:(DE-Juel1)ISB-2-20090406
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-Juel1)ICS-6-20110106
981 _ _ |a I:(DE-Juel1)IBI-7-20200312
981 _ _ |a I:(DE-Juel1)ISB-2-20090406
981 _ _ |a I:(DE-Juel1)ICS-6-20110106


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21