LAURA ATTARDI

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi request reprint Activation of the p53-dependent G1 checkpoint response in mouse embryo fibroblasts depends on the specific DNA damage inducer
    Laura D Attardi
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Oncogene 23:973-80. 2004
  2. ncbi request reprint Pathways connecting telomeres and p53 in senescence, apoptosis, and cancer
    Steven E Artandi
    Department of Medicine, Division of Hematology and Cancer Biology Program, Stanford University School of Medicine, Stanford, CA 94305, USA
    Biochem Biophys Res Commun 331:881-90. 2005
  3. ncbi request reprint Probing p53 biological functions through the use of genetically engineered mouse models
    Laura D Attardi
    Department of Radiation Oncology and Genetics, Stanford University School of Medicine, CCSR South, CA 94305 5152, USA
    Mutat Res 576:4-21. 2005
  4. pmc Unimpaired skin carcinogenesis in Desmoglein 3 knockout mice
    Sylvain Baron
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 7:e50024. 2012
  5. pmc Loss of the p53/p63 regulated desmosomal protein Perp promotes tumorigenesis
    VERONICA G BEAUDRY
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University School of Medicine, Stanford, California, USA
    PLoS Genet 6:e1001168. 2010
  6. pmc Loss of the desmosomal component perp impairs wound healing in vivo
    VERONICA G BEAUDRY
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Dermatol Res Pract 2010:759731. 2010
  7. pmc Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer
    Rachel L Dusek
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Center for Clinical Sciences Research Room 1255, 269 Campus Drive, Stanford, CA 94305, USA
    Breast Cancer Res 14:R65. 2012
  8. ncbi request reprint The role of apoptosis in cancer development and treatment response
    J Martin Brown
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford, California 94305, USA
    Nat Rev Cancer 5:231-7. 2005
  9. ncbi request reprint The p53QS transactivation-deficient mutant shows stress-specific apoptotic activity and induces embryonic lethality
    Thomas M Johnson
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, California 94305, USA
    Nat Genet 37:145-52. 2005
  10. ncbi request reprint The role of p53-mediated apoptosis as a crucial anti-tumor response to genomic instability: lessons from mouse models
    Laura D Attardi
    Stanford University School of Medicine, Departments of Radiation Oncology and Genetics, CCSR South, Room 1255, 269 Campus Drive, Stanford, CA 94305 5152, USA
    Mutat Res 569:145-57. 2005

Collaborators

Detail Information

Publications25

  1. ncbi request reprint Activation of the p53-dependent G1 checkpoint response in mouse embryo fibroblasts depends on the specific DNA damage inducer
    Laura D Attardi
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305 5152, USA
    Oncogene 23:973-80. 2004
    ..UVC, in contrast, induces a p53-independent G1 arrest response. Thus, the exact response of cells to DNA damage depends on the specific agent used...
  2. ncbi request reprint Pathways connecting telomeres and p53 in senescence, apoptosis, and cancer
    Steven E Artandi
    Department of Medicine, Division of Hematology and Cancer Biology Program, Stanford University School of Medicine, Stanford, CA 94305, USA
    Biochem Biophys Res Commun 331:881-90. 2005
    ..These fused chromosomes result in cycles of chromosome fusion-bridge-breakage, which can fuel cancer initiation, especially in epithelial tissues, by facilitating changes in gene copy number...
  3. ncbi request reprint Probing p53 biological functions through the use of genetically engineered mouse models
    Laura D Attardi
    Department of Radiation Oncology and Genetics, Stanford University School of Medicine, CCSR South, CA 94305 5152, USA
    Mutat Res 576:4-21. 2005
    ....
  4. pmc Unimpaired skin carcinogenesis in Desmoglein 3 knockout mice
    Sylvain Baron
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 7:e50024. 2012
    ..Continued unraveling of the roles of Dsg3 and other desmosomal constituents in carcinogenesis in different contexts will be important for ultimately improving cancer diagnosis, prognostication, and treatment...
  5. pmc Loss of the p53/p63 regulated desmosomal protein Perp promotes tumorigenesis
    VERONICA G BEAUDRY
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University School of Medicine, Stanford, California, USA
    PLoS Genet 6:e1001168. 2010
    ..An understanding of the factors affecting cancer progression is important for ultimately improving the diagnosis, prognostication, and treatment of cancer...
  6. pmc Loss of the desmosomal component perp impairs wound healing in vivo
    VERONICA G BEAUDRY
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Dermatol Res Pract 2010:759731. 2010
    ..Thus, Perp's role in promoting cell adhesion is essential for wound closure. Together, these studies suggest a role for desmosomal adhesion in efficient wound healing...
  7. pmc Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer
    Rachel L Dusek
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Center for Clinical Sciences Research Room 1255, 269 Campus Drive, Stanford, CA 94305, USA
    Breast Cancer Res 14:R65. 2012
    ..Given that p63 is essential for proper mammary gland development and that cell adhesion is fundamental for ensuring the proper architecture and function of the mammary epithelium, here we investigate Perp function in the mammary gland...
  8. ncbi request reprint The role of apoptosis in cancer development and treatment response
    J Martin Brown
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford, California 94305, USA
    Nat Rev Cancer 5:231-7. 2005
    ..Importantly, this suggests that other modes of cell death are involved in the response to therapy...
  9. ncbi request reprint The p53QS transactivation-deficient mutant shows stress-specific apoptotic activity and induces embryonic lethality
    Thomas M Johnson
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, California 94305, USA
    Nat Genet 37:145-52. 2005
    ..Taken together, these results suggest that p53 has different mechanisms of action depending on specific contextual cues, which may help to clarify the function of p53 in preventing cancer...
  10. ncbi request reprint The role of p53-mediated apoptosis as a crucial anti-tumor response to genomic instability: lessons from mouse models
    Laura D Attardi
    Stanford University School of Medicine, Departments of Radiation Oncology and Genetics, CCSR South, Room 1255, 269 Campus Drive, Stanford, CA 94305 5152, USA
    Mutat Res 569:145-57. 2005
    ..Thus p53-mediated apoptosis provides a crucial tumor suppressive mechanism to eliminate cells succumbing to genomic instability...
  11. pmc In vivo analysis of p53 tumor suppressor function using genetically engineered mouse models
    Daniela Kenzelmann Broz
    Department of Radiation Oncology, Stanford University School of Medicine, CA 94305, USA
    Carcinogenesis 31:1311-8. 2010
    ..These sophisticated p53 mouse models have taught us important lessons, and new mouse models will certainly continue to reveal interesting and perhaps surprising aspects of p53's complex biology...
  12. pmc Developmental context determines latency of MYC-induced tumorigenesis
    Shelly Beer
    Division of Oncology, Department of Medicine, Stanford University, Stanford, California, USA
    PLoS Biol 2:e332. 2004
    ..Adult somatic cells have evolved mechanisms to prevent individual oncogenes from initiating cellular growth, DNA replication, and mitotic cellular division alone, thereby preventing any single genetic event from inducing tumorigenesis...
  13. pmc The metastasis-associated gene Prl-3 is a p53 target involved in cell-cycle regulation
    Shashwati Basak
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Mol Cell 30:303-14. 2008
    ..Our findings highlight key dose-dependent functions of Prl-3 in both positive and negative regulation of cell-cycle progression and provide insight into Prl-3's role in cancer progression...
  14. ncbi request reprint A healthy tan?
    Gregory Barsh
    Stanford University School of Medicine, Stanford, CA, USA
    N Engl J Med 356:2208-10. 2007
  15. pmc Genome-wide analysis of p53 under hypoxic conditions
    Ester M Hammond
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University, Stanford, CA 94303 5152, USA
    Mol Cell Biol 26:3492-504. 2006
    ..This study defines a new role for residues 53 and 54 of p53 in regulating transrepression and demonstrates that 25-26 and 53-54 work in the same pathway to induce apoptosis through gene repression...
  16. ncbi request reprint Mice lacking the p53/p63 target gene Perp are resistant to papilloma development
    Michelle R Marques
    Department of Radiation Oncology, Division of Radiation and Cancer Biology, Stanford University School of Medicine, Stanford, California 94305, USA
    Cancer Res 65:6551-6. 2005
    ..These studies indicate that in certain contexts, Perp is required for efficient carcinogenesis and suggest a role for intact cell-cell adhesion in supporting tumor development in these settings...
  17. ncbi request reprint Perp is a mediator of p53-dependent apoptosis in diverse cell types
    Rebecca A Ihrie
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Curr Biol 13:1985-90. 2003
    ..In addition, we show that Perp is not required for proliferation-associated functions of p53. Thus, Perp selectively mediates the p53 apoptotic response, and the requirement for Perp is dictated by cellular context...
  18. ncbi request reprint p53QS: an old mutant teaches us new tricks
    Thomas M Johnson
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, USA
    Cell Cycle 4:731-4. 2005
    ..This p53QS mutant mouse strain represents a powerful means to dissect p53 function in vivo...
  19. pmc Differential PERP regulation by TP63 mutants provides insight into AEC pathogenesis
    VERONICA G BEAUDRY
    Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, 269 Campus Drive, Stanford, CA 94305 5152, USA
    Am J Med Genet A 149:1952-7. 2009
    ..Elucidating how specific TP63 target genes contribute to the pathogenesis of AEC will ultimately help design novel approaches to diagnose and treat AEC...
  20. pmc Ribosomal mutations cause p53-mediated dark skin and pleiotropic effects
    Kelly A McGowan
    Department of Genetics, Division of Radiation and CancerBiology, Stanford University, Stanford, California 94305, USA
    Nat Genet 40:963-70. 2008
    ....
  21. pmc Knockin mice expressing a chimeric p53 protein reveal mechanistic differences in how p53 triggers apoptosis and senescence
    Thomas M Johnson
    Departments of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 105:1215-20. 2008
    ..Our study highlights the central role of p53 transactivation for senescence while suggesting that transactivation is insufficient for apoptosis, and provides insight into the mechanisms by which p53 serves as a tumor suppressor...
  22. pmc Increased sensitivity to UV radiation in mice with a p53 point mutation at Ser389
    Wendy Bruins
    Laboratory of Toxicology, Pathology and Genetics, National Institute of Public Health and Environment RIVM, Bilthoven, The Netherlands
    Mol Cell Biol 24:8884-94. 2004
    ..Moreover, p53.S389A mice show increased sensitivity to UV-induced skin tumor development, signifying the importance of serine 389 phosphorylation for the tumor-suppressive function of p53...
  23. ncbi request reprint Dominant-negative but not gain-of-function effects of a p53.R270H mutation in mouse epithelium tissue after DNA damage
    Susan W P Wijnhoven
    Laboratory of Toxicology, Pathology and Genetics, National Institute of Public Health and the Environment, Bilthoven, The Netherlands
    Cancer Res 67:4648-56. 2007
    ..R270H were not detected in skin epithelium. Apparently, dominant-negative and gain-of-function effects of mutant p53 are highly tissue specific and become most manifest upon stabilization of p53 after DNA damage...
  24. ncbi request reprint Multiple response elements and differential p53 binding control Perp expression during apoptosis
    Elizabeth E Reczek
    Department of Biology and Center for Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
    Mol Cancer Res 1:1048-57. 2003
    ..These results provide mechanistic insight into the selective expression of Perp during apoptosis and may provide a useful model for studying the p53-dependent cell cycle arrest versus apoptosis decision...
  25. ncbi request reprint Conquering the complexity of p53
    Laura D Attardi
    Nat Genet 36:7-8. 2004

Research Grants15

  1. Characterization of the p53 Apoptotic Target Gene PERP
    Laura D Attardi; Fiscal Year: 2010
    ..An understanding of the factors affecting cancer progression ultimately will be important for better diagnosis, prognosis and therapy. ..
  2. Characterization of Siva in Nervous System Development and Apoptosis
    LAURA ATTARDI; Fiscal Year: 2007
    ..Moreover, because of its role in neuronal apoptosis, Siva represents a promising therapeutic target for treating diseases characterized by excessive neuronal cell death. ..
  3. Characterization of the p53 Apoptotic Target Gene PERP
    LAURA ATTARDI; Fiscal Year: 2007
    ..An understanding of the factors affecting cancer progression ultimately will be important for better diagnosis, prognosis and therapy. ..
  4. Characterization of the Desmosome Protein Perp
    LAURA ATTARDI; Fiscal Year: 2007
    ..Together, these approaches will provide an understanding of how Perp, desmosomes, and p63 contribute to both epithelial integrity and ectodermal appendage function, and how their dysfunction leads to disease. ..
  5. Characterization of the Desmosome Protein Perp
    Laura D Attardi; Fiscal Year: 2010
    ..Together, these approaches will provide an understanding of how Perp, desmosomes, and p63 contribute to both epithelial integrity and ectodermal appendage function, and how their dysfunction leads to disease. ..
  6. Characterization of the Desmosome Protein Perp
    LAURA ATTARDI; Fiscal Year: 2009
    ..Together, these approaches will provide an understanding of how Perp, desmosomes, and p63 contribute to both epithelial integrity and ectodermal appendage function, and how their dysfunction leads to disease. ..
  7. Characterization of the p53 Apoptotic Target Gene PERP
    LAURA ATTARDI; Fiscal Year: 2009
    ..An understanding of the factors affecting cancer progression ultimately will be important for better diagnosis, prognosis and therapy. ..
  8. Characterization of the p53 Apoptotic Target Gene PERP
    LAURA ATTARDI; Fiscal Year: 2006
    ..abstract_text> ..
  9. Characterization of the p53 Apoptotic Target Gene PERP
    LAURA ATTARDI; Fiscal Year: 2005
    ..abstract_text> ..
  10. Characterization of the p53 Apoptotic Target Gene PERP
    LAURA ATTARDI; Fiscal Year: 2004
    ..abstract_text> ..
  11. Characterization of the p53 Apoptotic Target Gene PERP
    LAURA ATTARDI; Fiscal Year: 2003
    ..abstract_text> ..
  12. Characterization of the p53 Apoptotic Target Gene PERP
    LAURA ATTARDI; Fiscal Year: 2002
    ..abstract_text> ..