Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (30)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Schulze, K. M. M.
Right arrow Articles by Hanenberg, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schulze, K. M. M.
Right arrow Articles by Hanenberg, H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Molecular Genetics, 2002, Vol. 11, No. 1 69-76
© 2002 Oxford University Press

Transduction of wild-type merlin into human schwannoma cells decreases schwannoma cell growth and induces apoptosis

K. M. M. Schulze, C. O. Hanemann2,+, H. W. Müller and H. Hanenberg1

Molecular Neurobiology Laboratory, Department of Neurology and 1Department of Pediatric Hematology/Oncology, Heinrich-Heine University Medical Center, Düsseldorf, Germany and 2Zentrum für klinische Forschung, Department of Neurology, University of Ulm, Ulm, Germany

Mutations in both alleles of the tumour suppressor gene coding for merlin/schwannomin, an ERM family protein, cause the hereditary disease neurofibromatosis type 2 (NF2). NF2 is characterized by the development of multiple nervous system tumours especially vestibular schwannomas. Efficient oncoretrovirus-mediated gene transfer of different merlin constructs was used to stably re-express wild-type merlin in primary cells derived from human schwannomas. Using two-parameter FACS analysis we show that expression of wild-type merlin in NF2 cells led to significant reduction of proliferation and G0/G1 arrest in transduced schwannoma cells. In addition, we show increased apoptosis of schwannoma cells transduced with wild-type merlin. Our findings in primary schwannoma cells from NF2 patients strongly support the hypothesis of merlin acting as a tumour suppressor and may help in understanding development of human schwannomas in NF2.

+ To whom correspondence should be addressed. Tel: +49 731 50033645; Fax: +49 731 50033609; Email: oliver.hanemann@medizin.uni-ulm.de


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Cancer Res.Home page
M. Okada, Y. Wang, S.-W. Jang, X. Tang, L. M. Neri, and K. Ye
Akt Phosphorylation of Merlin Enhances Its Binding to Phosphatidylinositols and Inhibits the Tumor-Suppressive Activities of Merlin
Cancer Res., May 1, 2009; 69(9): 4043 - 4051.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
S. Ammoun, C. Flaiz, N. Ristic, J. Schuldt, and C. O. Hanemann
Dissecting and Targeting the Growth Factor-Dependent and Growth Factor-Independent Extracellular Signal-Regulated Kinase Pathway in Human Schwannoma
Cancer Res., July 1, 2008; 68(13): 5236 - 5245.
[Abstract] [Full Text] [PDF]


Home page
BrainHome page
C. O. Hanemann
Magic but treatable? Tumours due to loss of Merlin
Brain, March 1, 2008; 131(3): 606 - 615.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
H. Lee, D. Kim, H. C. Dan, E. L. Wu, T. M. Gritsko, C. Cao, S. V. Nicosia, E. A. Golemis, W. Liu, D. Coppola, et al.
Identification and Characterization of Putative Tumor Suppressor NGB, a GTP-Binding Protein That Interacts with the Neurofibromatosis 2 Protein
Mol. Cell. Biol., March 15, 2007; 27(6): 2103 - 2119.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
G.-H. Xiao, R. Gallagher, J. Shetler, K. Skele, D. A. Altomare, R. G. Pestell, S. Jhanwar, and J. R. Testa
The NF2 Tumor Suppressor Gene Product, Merlin, Inhibits Cell Proliferation and Cell Cycle Progression by Repressing Cyclin D1 Expression
Mol. Cell. Biol., March 15, 2005; 25(6): 2384 - 2394.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
R. Rong, X. Tang, D. H. Gutmann, and K. Ye
Neurofibromatosis 2 (NF2) tumor suppressor merlin inhibits phosphatidylinositol 3-kinase through binding to PIKE-L
PNAS, December 28, 2004; 101(52): 18200 - 18205.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
J. T. Stickney, W. C. Bacon, M. Rojas, N. Ratner, and W. Ip
Activation of the Tumor Suppressor Merlin Modulates Its Interaction with Lipid Rafts
Cancer Res., April 15, 2004; 64(8): 2717 - 2724.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
H. Kim, N.-J. Kwak, J. Y. Lee, B. H. Choi, Y. Lim, Y. J. Ko, Y.-H. Kim, P.-W. Huh, K.-H. Lee, H. K. Rha, et al.
Merlin Neutralizes the Inhibitory Effect of Mdm2 on p53
J. Biol. Chem., February 27, 2004; 279(9): 7812 - 7818.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
K. Kaempchen, K. Mielke, T. Utermark, S. Langmesser, and C. O. Hanemann
Upregulation of the Rac1/JNK signaling pathway in primary human schwannoma cells
Hum. Mol. Genet., June 1, 2003; 12(11): 1211 - 1221.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
C.-X. Sun, C. Haipek, D. R. Scoles, S. M. Pulst, M. Giovannini, M. Komada, and D. H. Gutmann
Functional analysis of the relationship between the neurofibromatosis 2 tumor suppressor and its binding partner, hepatocyte growth factor-regulated tyrosine kinase substrate
Hum. Mol. Genet., December 1, 2002; 11(25): 3167 - 3178.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
M. Kressel and B. Schmucker
Nucleocytoplasmic transfer of the NF2 tumor suppressor protein merlin is regulated by exon 2 and a CRM1-dependent nuclear export signal in exon 15
Hum. Mol. Genet., September 15, 2002; 11(19): 2269 - 2278.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.