TY  - GEN
AB  - This study investigates the role of p73 in epidermal carcinogenesis and DNA damage responses within the context of p53 family signaling. Loss of p73 promoted malignant conversion of keratinocytes to squamous cell carcinoma and conferred resistance to ionizing radiation, effects reversible by reconstitution of TAp73α but not ΔNp73α. p73 was shown to functionally cooperate with transcriptionally active p63 isoforms to regulate cell cycle arrest and gene expression, while its tumor suppressive role was uncoupled from radiation sensitivity. These findings highlight p73 as a critical regulator of p53 family balance, tumor suppression, and treatment response.
AD  - Oregon Health and Science University
AU  - Johnson, Jodi
DA  - 2007
DO  - 10.6083/M42F7KD0
DO  - DOI
ED  - Martin-Kulesz, Molly
ED  - Advisor
ED  - Mentor
ID  - 309
KW  - Neoplastic Processes
KW  - DNA Damage
KW  - Keratinocytes
KW  - Radiation
KW  - DNA-Binding Proteins
KW  - Carcinogenesis
KW  - DNA Repair
KW  - Epithelial Cells
KW  - Tumor Suppressor Protein p53
KW  - Radiation, Nonionizing
KW  - Ultraviolet Rays
KW  - Radiation, Ionizing
KW  - p63
KW  - p73
KW  - squamous cell carcinogenesis
L1  - https://digitalcollections.ohsu.edu/record/309/files/309_etd.pdf
L2  - https://digitalcollections.ohsu.edu/record/309/files/309_etd.pdf
L4  - https://digitalcollections.ohsu.edu/record/309/files/309_etd.pdf
LK  - https://digitalcollections.ohsu.edu/record/309/files/309_etd.pdf
N2  - This study investigates the role of p73 in epidermal carcinogenesis and DNA damage responses within the context of p53 family signaling. Loss of p73 promoted malignant conversion of keratinocytes to squamous cell carcinoma and conferred resistance to ionizing radiation, effects reversible by reconstitution of TAp73α but not ΔNp73α. p73 was shown to functionally cooperate with transcriptionally active p63 isoforms to regulate cell cycle arrest and gene expression, while its tumor suppressive role was uncoupled from radiation sensitivity. These findings highlight p73 as a critical regulator of p53 family balance, tumor suppression, and treatment response.
PB  - Oregon Health and Science University
PY  - 2007
T1  - The p53 family interacting pathways in carcinogenesis and cellular response to DNA damage
TI  - The p53 family interacting pathways in carcinogenesis and cellular response to DNA damage
UR  - https://digitalcollections.ohsu.edu/record/309/files/309_etd.pdf
Y1  - 2007
ER  -