HYPOXIA-SPECIFIC STABILIZATION OF HIF-1ALPHA BY HUMAN PAPILLOMAVIRSUES

[1]  E. Rankin,et al.  The role of hypoxia-inducible factors in tumorigenesis , 2008, Cell Death and Differentiation.

[2]  C. Tzeng,et al.  Roles for hypoxia-regulated genes during cervical carcinogenesis: somatic evolution during the hypoxia-glycolysis-acidosis sequence. , 2008, Gynecologic oncology.

[3]  J. Archambault,et al.  Human papillomaviruses activate caspases upon epithelial differentiation to induce viral genome amplification , 2007, Proceedings of the National Academy of Sciences.

[4]  J. Walker,et al.  Human papillomavirus causes an angiogenic switch in keratinocytes which is sufficient to alter endothelial cell behavior. , 2007, Virology.

[5]  I. Lascombe,et al.  The human papillomavirus type 18 E6 oncoprotein induces Vascular Endothelial Growth Factor 121 (VEGF121) transcription from the promoter through a p53-independent mechanism. , 2007, Experimental cell research.

[6]  T. Libermann,et al.  Human Papillomavirus Type 16 E7 Oncoprotein Associates with the Cullin 2 Ubiquitin Ligase Complex, Which Contributes to Degradation of the Retinoblastoma Tumor Suppressor , 2007, Journal of Virology.

[7]  H. Federoff,et al.  In Cultured Astrocytes, p53 and MDM2 Do Not Alter Hypoxia-inducible Factor-1α Function Regardless of the Presence of DNA Damage* , 2007, Journal of Biological Chemistry.

[8]  A. Le,et al.  Overexpression of Human Papillomavirus Type 16 Oncoproteins Enhances Hypoxia-Inducible Factor 1α Protein Accumulation and Vascular Endothelial Growth Factor Expression in Human Cervical Carcinoma Cells , 2007, Clinical Cancer Research.

[9]  Paul Zhang,et al.  Oxygen levels in normal and previously irradiated human skin as assessed by EF5 binding. , 2006, The Journal of investigative dermatology.

[10]  J. Rader,et al.  Human papillomaviruses target the double-stranded RNA protein kinase pathway. , 2006, The Journal of general virology.

[11]  L. Zitvogel,et al.  Cancer despite immunosurveillance: immunoselection and immunosubversion , 2006, Nature Reviews Immunology.

[12]  Heidi L. Kenerson,et al.  Latent Kaposi's Sarcoma-Associated Herpesvirus Infection of Endothelial Cells Activates Hypoxia-Induced Factors , 2006, Journal of Virology.

[13]  Rosa Bernardi,et al.  PML inhibits HIF-1α translation and neoangiogenesis through repression of mTOR , 2006, Nature.

[14]  B. Brüne,et al.  Tumor hypoxia and cancer progression. , 2006, Cancer letters.

[15]  Margaret Ashcroft,et al.  Negative and positive regulation of HIF-1: a complex network. , 2005, Biochimica et biophysica acta.

[16]  L. Laimins,et al.  Role of the E1∧E4 Protein in the Differentiation-Dependent Life Cycle of Human Papillomavirus Type 31 , 2005, Journal of Virology.

[17]  A. Dejean,et al.  Human Papillomavirus Oncoprotein E7 Targets the Promyelocytic Leukemia Protein and Circumvents Cellular Senescence via the Rb and p53 Tumor Suppressor Pathways , 2005, Molecular and Cellular Biology.

[18]  M. Grace,et al.  Mechanisms of Human Papillomavirus-Induced Oncogenesis , 2004, Journal of Virology.

[19]  Y. Kitamoto,et al.  Expression of hypoxic-inducible factor 1alpha predicts metastasis-free survival after radiation therapy alone in stage IIIB cervical squamous cell carcinoma. , 2004, International journal of radiation oncology, biology, physics.

[20]  A. Wree,et al.  Lack of Correlation between Expression of HIF-1α Protein and Oxygenation Status in Identical Tissue Areas of Squamous Cell Carcinomas of the Uterine Cervix , 2004, Cancer Research.

[21]  Michelle S. Longworth,et al.  Pathogenesis of Human Papillomaviruses in Differentiating Epithelia , 2004, Microbiology and Molecular Biology Reviews.

[22]  B. Brüne,et al.  p300 relieves p53-evoked transcriptional repression of hypoxia-inducible factor-1 (HIF-1). , 2004, The Biochemical journal.

[23]  N. Chandel,et al.  Follicle-stimulating Hormone Activation of Hypoxia-inducible Factor-1 by the Phosphatidylinositol 3-Kinase/AKT/Ras Homolog Enriched in Brain (Rheb)/Mammalian Target of Rapamycin (mTOR) Pathway Is Necessary for Induction of Select Protein Markers of Follicular Differentiation* , 2004, Journal of Biological Chemistry.

[24]  D. Donner,et al.  Expression of human papillomavirus type 16 E6 and E7 oncoproteins in primary foreskin keratinocytes is sufficient to alter the expression of angiogenic factors , 2004, Oncogene.

[25]  M. Ashcroft,et al.  Growth Factor-Mediated Induction of HDM2 Positively Regulates Hypoxia-Inducible Factor 1α Expression , 2004, Molecular and Cellular Biology.

[26]  L. Laimins,et al.  Roles of the E6 and E7 Proteins in the Life Cycle of Low-Risk Human Papillomavirus Type 11 , 2004, Journal of Virology.

[27]  R. Pötter,et al.  Overexpression of hypoxia-inducible factor 1alpha indicates diminished response to radiotherapy and unfavorable prognosis in patients receiving radical radiotherapy for cervical cancer. , 2003, Clinical cancer research : an official journal of the American Association for Cancer Research.

[28]  D. Klumpp,et al.  Human Papillomavirus Type 31 E5 Protein Supports Cell Cycle Progression and Activates Late Viral Functions upon Epithelial Differentiation , 2003, Journal of Virology.

[29]  P. M. O'Brien,et al.  Evasion of host immunity directed by papillomavirus-encoded proteins. , 2002, Virus research.

[30]  D. McCance,et al.  Down Regulation of the Interleukin-8 Promoter by Human Papillomavirus Type 16 E6 and E7 through Effects on CREB Binding Protein/p300 and P/CAF , 2002, Journal of Virology.

[31]  K. Münger,et al.  Stabilization and functional impairment of the tumor suppressor p53 by the human papillomavirus type 16 E7 oncoprotein. , 2002, Virology.

[32]  D. Spandau,et al.  E5 Protein of Human Papillomavirus Type 16 Protects Human Foreskin Keratinocytes from UV B-Irradiation-Induced Apoptosis , 2002, Journal of Virology.

[33]  M. Béquet-Romero,et al.  Angiogenesis modulators expression in culture cell lines positives for HPV-16 oncoproteins. , 2000, Biochemical and biophysical research communications.

[34]  D. Mukhopadhyay,et al.  Oncogenes and tumor angiogenesis: the HPV-16 E6 oncoprotein activates the vascular endothelial growth factor (VEGF) gene promoter in a p53 independent manner , 2000, Oncogene.

[35]  R. Schlegel,et al.  E5 Oncoprotein Mutants Activate Phosphoinositide 3-Kinase Independently of Platelet-derived Growth Factor Receptor Activation* , 2000, The Journal of Biological Chemistry.

[36]  D. Hanahan,et al.  The Hallmarks of Cancer , 2000, Cell.

[37]  P. Stern,et al.  The Human Papillomavirus (HPV) 16 E2 Protein Induces Apoptosis in the Absence of Other HPV Proteins and via a p53-dependent Pathway* , 2000, The Journal of Biological Chemistry.

[38]  G. Semenza,et al.  Regulation of tumor angiogenesis by p53-induced degradation of hypoxia-inducible factor 1alpha. , 2000, Genes & development.

[39]  M. Grace,et al.  Expression of the HPV E7 oncoprotein mimics but does not evoke a p53-dependent cellular DNA damage response pathway. , 1999, Virology.

[40]  L. Laimins,et al.  Human papillomavirus oncoproteins alter differentiation-dependent cell cycle exit on suspension in semisolid medium. , 1998, Virology.

[41]  L. Neckers,et al.  Stabilization of wild-type p53 by hypoxia-inducible factor 1α , 1998, Nature.

[42]  L. Laimins,et al.  Human Papillomavirus Oncoproteins E6 and E7 Independently Abrogate the Mitotic Spindle Checkpoint , 1998, Journal of Virology.

[43]  D. Hanahan,et al.  Cross-species comparison of angiogenesis during the premalignant stages of squamous carcinogenesis in the human cervix and K14-HPV16 transgenic mice. , 1997, Cancer research.

[44]  D. Hanahan,et al.  Patterns and Emerging Mechanisms of the Angiogenic Switch during Tumorigenesis , 1996, Cell.

[45]  K. Smith-McCune,et al.  Demonstration and characterization of the angiogenic properties of cervical dysplasia. , 1994, Cancer research.

[46]  C. Woodworth,et al.  Recombinant retroviruses encoding human papillomavirus type 18 E6 and E7 genes stimulate proliferation and delay differentiation of human keratinocytes early after infection. , 1992, Oncogene.

[47]  G. Demers,et al.  The E7 gene of human papillomavirus type 16 is sufficient for immortalization of human epithelial cells , 1991, Journal of virology.

[48]  Arnold J. Levine,et al.  The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53 , 1990, Cell.

[49]  T. Golub,et al.  In vitro differentiation of epithelial cells from cervical neoplasias resembles in vivo lesions. , 1990, Oncogene.

[50]  D. McCance,et al.  Immortalization and altered differentiation of human keratinocytes in vitro by the E6 and E7 open reading frames of human papillomavirus type 18 , 1990, Journal of virology.

[51]  M. Braun,et al.  Structural and transcriptional analysis of human papillomavirus type 16 sequences in cervical carcinoma cell lines , 1987, Journal of virology.

[52]  S. Landolfo,et al.  Interaction between inflammation and angiogenesis during different stages of cervical carcinogenesis. , 2008, Gynecologic oncology.

[53]  Rosa Bernardi,et al.  PML inhibits HIF-1alpha translation and neoangiogenesis through repression of mTOR. , 2006, Nature.

[54]  L. Laimins,et al.  Differentiation of HPV-containing cells using organotypic "raft" culture or methylcellulose. , 2005, Methods in molecular medicine.

[55]  C. Meyers,et al.  Analysis of HPV transcription by RPA. , 2005, Methods in molecular medicine.

[56]  R. Abraham.  mTOR as a positive regulator of tumor cell responses to hypoxia. , 2004, Current topics in microbiology and immunology.

[57]  Daniel J Brat,et al.  Genetic modulation of hypoxia induced gene expression and angiogenesis: relevance to brain tumors. , 2003, Frontiers in bioscience : a journal and virtual library.

[58]  H. Hausen,et al.  Papillomaviruses in human cancers , 1999, Proceedings of the Association of American Physicians.

[59]  H. zur Hausen,et al.  Papillomavirus infections--a major cause of human cancers. , 1996, Biochimica et biophysica acta.

[60]  C. Meyers,et al.  In vitro systems for the study and propagation of human papillomaviruses. , 1994, Current topics in microbiology and immunology.