Differential regulation of different human papilloma virus variants by the POU family transcription factor Brn-3a
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A. Singer | D. Latchman | V. Budhram-Mahadeo | D. Gascoyne | J. Cason | M. Sindos | B. Ripley | D. Ndisang | D. Faulkes | S. -. Lee | D. S. Latchman | Duncan Gascoyne | Sonia A. Lee | Barry J. Ripley | Michael Sindos | Albert Singer | John Cason
[1] K. Hagino-Yamagishi,et al. [Oncogene]. , 2019, Gan to kagaku ryoho. Cancer & chemotherapy.
[2] V. Budhram-Mahadeo,et al. Expression of the Brn-3b transcription factor correlates with expression of HSP-27 in breast cancer biopsies and is required for maximal activation of the HSP-27 promoter. , 2005, Cancer research.
[3] D. Isenberg,et al. Elevated expression of the Brn-3a and Brn-3b transcription factors in systemic lupus erythematosus correlates with antibodies to Brn-3 and overexpression of Hsp90. , 2005, Arthritis and rheumatism.
[4] D. Latchman,et al. Coexpression of Brn‐3a POU protein with p53 in a population of neuronal progenitor cells is associated with differentiation and protection against apoptosis , 2004, Journal of neuroscience research.
[5] D. Latchman,et al. The effects of Brn-3a on neuronal differentiation and apoptosis are differentially modulated by EWS and its oncogenic derivative EWS/Fli-1 , 2004, Oncogene.
[6] A. Singer,et al. Measurement of Brn-3a levels in Pap smears provides a novel diagnostic marker for the detection of cervical neoplasia. , 2003, Gynecologic oncology.
[7] D. Latchman,et al. The Brn-3a transcription factor plays a key role in regulating the growth of cervical cancer cells in vivo , 2001, Oncogene.
[8] C. Woodman,et al. Natural history of cervical human papillomavirus infection in young women: a longitudinal cohort study , 2001, The Lancet.
[9] A. Miller. Natural history of cervical human papillomavirus infections , 2001, The Lancet.
[10] T. Rohan,et al. Molecular variants of human papillomavirus types 16 and 18 preferentially associated with cervical neoplasia. , 2000, The Journal of general virology.
[11] C. Wheeler,et al. Sequence analysis of the long control region of human papillomavirus type 16 variants and functional consequences for P97 promoter activity. , 2000, The Journal of general virology.
[12] J. Best,et al. Cervical lesions are associated with human papillomavirus type 16 intratypic variants that have high transcriptional activity and increased usage of common mammalian codons. , 2000, The Journal of general virology.
[13] A. Singer,et al. Widespread elevated expression of the human papilloma virus (HPV)-activating cellular transcription factor Brn-3a in the cervix of women with CIN3 (cervical intraepithelial neoplasia stage 3). , 2000, Clinical science.
[14] 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.
[15] C. Meijer,et al. Relation of human papilloma virus status to cervical lesions and consequences for cervical-cancer screening: a prospective study , 1999, The Lancet.
[16] A. Singer,et al. The HPV-activating cellular transcription factor Brn-3a is overexpressed in CIN3 cervical lesions. , 1998, The Journal of clinical investigation.
[17] R. Burk,et al. Natural history of cervicovaginal papillomavirus infection in young women , 1998 .
[18] M. Rosenfeld,et al. POU domain family values: flexibility, partnerships, and developmental codes. , 1997, Genes & development.
[19] D. Hanahan,et al. A transition in transcriptional activation by the glucocorticoid and retinoic acid receptors at the tumor stage of dermal fibrosarcoma development. , 1995, The EMBO journal.
[20] D. Latchman,et al. The opposite and antagonistic effects of the closely related POU family transcription factors Brn-3a and Brn-3b on the activity of a target promoter are dependent on differences in the POU domain , 1994, Molecular and cellular biology.
[21] S Wacholder,et al. Epidemiologic evidence showing that human papillomavirus infection causes most cervical intraepithelial neoplasia. , 1993, Journal of the National Cancer Institute.
[22] C. Verrijzer,et al. POU domain transcription factors. , 1993, Biochimica et biophysica acta.
[23] D. Latchman,et al. A novel POU family transcription factor is closely related to Brn-3 but has a distinct expression pattern in neuronal cells. , 1992, Nucleic acids research.
[24] D. Latchman,et al. The constitutively expressed octamer binding protein OTF-1 and a novel octamer binding protein expressed specifically in cervical cells bind to an octamer-related sequence in the human papillomavirus 16 enhancer. , 1991, Nucleic acids research.
[25] H. Nakshatri,et al. Ubiquitous and cell-type-specific protein interactions with human papillomavirus type 16 and type 18 enhancers. , 1990, Virology.
[26] H. Bernard,et al. Transcription of the transforming genes of the oncogenic human papillomavirus-16 is stimulated by tumor promotors through AP1 binding sites. , 1990, Nucleic acids research.
[27] H. Bernard,et al. Progesterone and glucocorticoid response elements occur in the long control regions of several human papillomaviruses involved in anogenital neoplasia , 1989, Journal of virology.
[28] L. Swanson,et al. Expression of a large family of POU-domain regulatory genes in mammalian brain development , 1989, Nature.
[29] E. Winnacker,et al. Clusters of nuclear factor I binding sites identify enhancers of several papillomaviruses but alone are not sufficient for enhancer function. , 1989, Nucleic acids research.
[30] L. Turek,et al. Transcriptional regulation of the human papillomavirus‐16 E6‐E7 promoter by a keratinocyte‐dependent enhancer, and by viral E2 trans‐activator and repressor gene products: implications for cervical carcinogenesis. , 1987, The EMBO journal.
[31] H. Wesch,et al. HUMAN PAPILLOMAVIRUS INFECTIONS IN WOMEN WITH AND WITHOUT ABNORMAL CERVICAL CYTOLOGY , 1987, The Lancet.
[32] N. Maitland,et al. HUMAN PAPILLOMAVIRUS TYPE-16 HOMOLOGOUS DNA IN NORMAL HUMAN ECTOCERVIX , 1986, The Lancet.
[33] E. Burghardt. Microinvasive carcinoma in gynaecological pathology. , 1984, Clinics in obstetrics and gynaecology.
[34] L. Gissmann,et al. A papillomavirus DNA from a cervical carcinoma and its prevalence in cancer biopsy samples from different geographic regions. , 1983, Proceedings of the National Academy of Sciences of the United States of America.
[35] Calvin G. Barnes,et al. Arthritis and Rheumatism , 1966, The British journal of clinical practice.
[36] D. Smithers,et al. Cancer Research , 1972, Nature.
[37] V. Georgiev. Virology , 1955, Nature.