The effects of Brn-3a on neuronal differentiation and apoptosis are differentially modulated by EWS and its oncogenic derivative EWS/Fli-1

[1]  M. Vivanco,et al.  Glucocorticoids Inhibit Apoptosis during Fibrosarcoma Development by Transcriptionally Activating Bcl-xL * , 2003, The Journal of Biological Chemistry.

[2]  Y. Iwamoto,et al.  Identification of p21 WAF1/CIP1 as a Direct Target of EWS-Fli1 Oncogenic Fusion Protein* , 2003, The Journal of Biological Chemistry.

[3]  K. Wagner,et al.  The Wilms' tumor suppressor Wt1 encodes a transcriptional activator of the class IV POU-domain factor Pou4f2 (Brn-3b). , 2003, Gene.

[4]  A. Fukamizu,et al.  Cooperative Interaction of EWS with CREB-binding Protein Selectively Activates Hepatocyte Nuclear Factor 4-mediated Transcription* , 2003, The Journal of Biological Chemistry.

[5]  Yusuke Nakamura,et al.  The Id2 gene is a novel target of transcriptional activation by EWS-ETS fusion proteins in Ewing family tumors , 2002, Oncogene.

[6]  D. Latchman,et al.  The Brn-3a transcription factor inhibits the pro-apoptotic effect of p53 and enhances cell cycle arrest by differentially regulating the activity of the p53 target genes encoding Bax and p21CIP1/Waf1 , 2002, Oncogene.

[7]  T. Golub,et al.  Supplemental Information for , 2002 .

[8]  S. Welford,et al.  DNA Binding Domain-independent Pathways Are Involved in EWS/FLI1-mediated Oncogenesis* , 2001, The Journal of Biological Chemistry.

[9]  Christopher T Denny,et al.  Biology of EWS/ETS fusions in Ewing's family tumors , 2001, Oncogene.

[10]  O. Delattre,et al.  Analysis of the expression of cell cycle regulators in Ewing cell lines: EWS-FLI-1 modulates p57KIP2 and c-Myc expression , 2001, Oncogene.

[11]  M. Itoh,et al.  Involvement of the Pro-oncoprotein TLS (Translocated in Liposarcoma) in Nuclear Factor-κB p65-mediated Transcription as a Coactivator* , 2001, The Journal of Biological Chemistry.

[12]  D. Latchman,et al.  Brn-3a Activates the Expression of Bcl-xL and Promotes Neuronal Survival in Vivo as Well as in Vitro , 2001, Molecular and Cellular Neuroscience.

[13]  K. Tanaka,et al.  Downregulation and forced expression of EWS-Fli1 fusion gene results in changes in the expression of G 1 regulatory genes , 2001, British Journal of Cancer.

[14]  D. Latchman,et al.  The BRN-3A Transcription Factor Protects Sensory but Not Sympathetic Neurons from Programmed Cell Death/Apoptosis* , 2001, The Journal of Biological Chemistry.

[15]  H. Chansky,et al.  EWS·Fli-1 Fusion Protein Interacts with Hyperphosphorylated RNA Polymerase II and Interferes with Serine-Arginine Protein-mediated RNA Splicing* , 2000, The Journal of Biological Chemistry.

[16]  B. Weber,et al.  The Brn-3b POU family transcription factor represses expression of the BRCA-1 anti-oncogene in breast cancer cells , 1999, Oncogene.

[17]  D. Latchman,et al.  The Brn-3a Transcription Factor Plays a Critical Role in Regulating Human Papilloma Virus Gene Expression and Determining the Growth Characteristics of Cervical Cancer Cells* , 1999, The Journal of Biological Chemistry.

[18]  C. Denny,et al.  Divergent Ewing's sarcoma EWS/ETS fusions confer a common tumorigenic phenotype on NIH3T3 cells , 1999, Oncogene.

[19]  M. Roussel,et al.  Transforming activity of EWS/FLI is not strictly dependent upon DNA-binding activity , 1999, Oncogene.

[20]  Erica A Golemis,et al.  Oncogenic EWS-Fli1 interacts with hsRPB7, a subunit of human RNA polymerase II , 1998, Oncogene.

[21]  D. Latchman,et al.  A single residue within the homeodomain of the Brn‐3 POU family transcription factors determines whether they activate or repress the SNAP‐25 promoter , 1997, Neuroreport.

[22]  M. Ouchida,et al.  Inhibition of apoptosis by normal and aberrant Fli-1 and erg proteins involved in human solid tumors and leukemias , 1997, Oncogene.

[23]  P. Sawchenko,et al.  Requirement for Brn-3.0 in differentiation and survival of sensory and motor neurons , 1996, Nature.

[24]  J. Nathans,et al.  Targeted deletion of the mouse POU domain gene Brn-3a causes selective loss of neurons in the brainstem and trigeminal ganglion, uncoordinated limb movement, and impaired suckling. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[25]  Michael G. Rosenfeld,et al.  Role of transcription factors a Brn-3.1 and Brn-3.2 in auditory and visual system development , 1996, Nature.

[26]  T. Möröy,et al.  Regulation of Neurite Outgrowth and SNAP-25 Gene Expression by the Brn-3a Transcription Factor (*) , 1995, The Journal of Biological Chemistry.

[27]  M. Roussel,et al.  DNA-binding and transcriptional activation properties of the EWS-FLI-1 fusion protein resulting from the t(11;22) translocation in Ewing sarcoma , 1994, Molecular and cellular biology.

[28]  G. Thomas,et al.  Genomic structure of the EWS gene and its relationship to EWSR1, a site of tumor-associated chromosome translocation. , 1993, Genomics.