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 (36)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Roberts, T.
Right arrow Articles by Cowell, J. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Roberts, T.
Right arrow Articles by Cowell, J. K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Molecular Genetics, Vol 7, 1169-1178, Copyright © 1998 by Oxford University Press

ARTICLES

NB4S, a member of the TBC1 domain family of genes, is truncated as a result of a constitutional t(1;10)(p22;q21) chromosome translocation in a patient with stage 4S neuroblastoma

T Roberts, O Chernova and JK Cowell
Department of Neurosciences-NC30, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

Molecular cloning of the breakpoints of a t(1;10)(p22q21) constitutional translocation breakpoint in a patient with stage 4S neuroblastoma has identified two genes which are fused in-frame to generate a novel gene. The 1p22 gene, which we have called NB4S , encodes a 7.5 kb transcript with an 810 amino acid open reading frame and is expressed in a wide variety of tissues. NB4S has >88% homology with the mouse EVI -5 gene within the coding region and shows strong homology over a 200 amino acid region with TBC1 box motif genes involved in cell growth and differentiation. The C-teminal end of the protein contains a number of coiled coil domains, indicating a possible protein-protein binding function. The chromosome 10 breakpoint interrupts a novel transcript (TRNG10) which could only be detected in tumor cells. This transcript has no exon/intron structure or significant open reading frame, suggesting that it is a structural RNA which is transcribed but not translated. The chromosome rearrangement creates a fusion gene product which combines the TBC1 motif of NB4S with a polyadenylation signal from TRNG10 , potentially generating a truncated protein with oncogenic properties.
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
 Mol Biol EvolHome page
K. Vandepoele, V. Andries, and F. van Roy
The NBPF1 Promoter Has Been Recruited from the Unrelated EVI5 Gene Before Simian Radiation
Mol. Biol. Evol., June 1, 2009; 26(6): 1321 - 1332.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
K. V. Prasanth and D. L. Spector
Eukaryotic regulatory RNAs: an answer to the 'genome complexity' conundrum
Genes & Dev., January 1, 2007; 21(1): 11 - 42.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
I. M. Veltman, L. A. Vreede, J. Cheng, L. H.J. Looijenga, B. Janssen, E. F.P.M. Schoenmakers, E. T.H. Yeh, and A. G. van Kessel
Fusion of the SUMO/Sentrin-specific protease 1 gene SENP1 and the embryonic polarity-related mesoderm development gene MESDC2 in a patient with an infantile teratoma and a constitutional t(12;15)(q13;q25)
Hum. Mol. Genet., July 15, 2005; 14(14): 1955 - 1963.
[Abstract] [Full Text] [PDF]

Home page
 J. Mol. Diagn.Home page
G. Troen, V. Nygaard, T.-K. Jenssen, I. M. Ikonomou, A. Tierens, E. Matutes, A. Gruszka-Westwood, D. Catovsky, O. Myklebost, G. Lauritzsen, et al.
Constitutive Expression of the AP-1 Transcription Factors c-jun, junD, junB, and c-fos and the Marginal Zone B-Cell Transcription Factor Notch2 in Splenic Marginal Zone Lymphoma
J. Mol. Diagn., November 1, 2004; 6(4): 297 - 307.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
M. S. Shin, T. N. Fredrickson, J. W. Hartley, T. Suzuki, K. Agaki, and H. C. Morse III
High-Throughput Retroviral Tagging for Identification of Genes Involved in Initiation and Progression of Mouse Splenic Marginal Zone Lymphomas
Cancer Res., July 1, 2004; 64(13): 4419 - 4427.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
H. Shen, T. Suzuki, D. J. Munroe, C. Stewart, L. Rasmussen, D. J. Gilbert, N. A. Jenkins, and N. G. Copeland
Common Sites of Retroviral Integration in Mouse Hematopoietic Tumors Identified by High-Throughput, Single Nucleotide Polymorphism-Based Mapping and Bacterial Artificial Chromosome Hybridization
J. Virol., December 20, 2002; 77(2): 1584 - 1588.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
M. L. Brandi, R. F. Gagel, A. Angeli, J. P. Bilezikian, P. Beck-Peccoz, C. Bordi, B. Conte-Devolx, A. Falchetti, R. G. Gheri, A. Libroia, et al.
CONSENSUS: Guidelines for Diagnosis and Therapy of MEN Type 1 and Type 2
J. Clin. Endocrinol. Metab., December 1, 2001; 86(12): 5658 - 5671.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
T. Nakamura, Y. Yamazaki, Y. Saiki, M. Moriyama, D. A. Largaespada, N. A. Jenkins, and N. G. Copeland
Evi9 Encodes a Novel Zinc Finger Protein That Physically Interacts with BCL6, a Known Human B-Cell Proto-Oncogene Product
Mol. Cell. Biol., May 1, 2000; 20(9): 3178 - 3186.
[Abstract] [Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
C. Heppner, M. Reincke, S. K. Agarwal, P. Mora, B. Allolio, A. L. Burns, A. M. Spiegel, and S. J. Marx
MEN1 Gene Analysis in Sporadic Adrenocortical Neoplasms
J. Clin. Endocrinol. Metab., January 1, 1999; 84(1): 216 - 219.
[Abstract] [Full Text]


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.