Zobrazeno 1 - 10
of 21
pro vyhledávání: '"Catherine A. Vaughan"'
Autor:
Catherine A. Vaughan, Shilpa Singh, Mark A. Subler, Jolene J. Windle, Kazushi Inoue, Elizabeth A. Fry, Raghavendra Pillappa, Steven R. Grossman, Brad Windle, W. Andrew Yeudall, Swati Palit Deb, Sumitra Deb
Publikováno v:
Nature Communications, Vol 12, Iss 1, Pp 1-19 (2021)
The mechanisms of how gain-of-function (GOF) mutant p53 drives carcinogenesis are unclear. Here, the authors show that a GOF mutant p53 requires its transactivation capability to induce mouse lung tumors and this is dependent on PLK3 phosphorylation
Externí odkaz:
https://doaj.org/article/54a056e3c31c4f638609e87d39e9e921
Autor:
Shilpa Singh, Brad Windle, Sumitra Deb, Elizabeth A. Fry, Jolene J. Windle, W. Andrew Yeudall, Kazushi Inoue, Swati Palit Deb, Catherine A. Vaughan, Steven R. Grossman, Mark A. Subler, Raghavendra Pillappa
Publikováno v:
Nature Communications
Nature Communications, Vol 12, Iss 1, Pp 1-19 (2021)
Nature Communications, Vol 12, Iss 1, Pp 1-19 (2021)
p53 mutations with single amino acid changes in cancer often lead to dominant oncogenic changes. Here, we have developed a mouse model of gain-of-function (GOF) p53-driven lung cancer utilizing conditionally active LSL p53-R172H and LSL K-Ras-G12D kn
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3001552fe338f8bbf14360dc3fb8e02d
http://europepmc.org/articles/PMC7846773
http://europepmc.org/articles/PMC7846773
Autor:
Catherine A. Vaughan, Shilpa Singh, Swati Palit Deb, Sumitra Deb, Steven R. Grossman, Rebecca Frum
Publikováno v:
Journal of Clinical Investigation. 127:1839-1855
Gain-of-function (GOF) p53 mutations are observed frequently in most intractable human cancers and establish dependency for tumor maintenance and progression. While some of the genes induced by GOF p53 have been implicated in more rapid cell prolifer
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::347785aaec3a5ca15511c0086ea995cb
https://doi.org/10.1172/jci87724
https://doi.org/10.1172/jci87724
Autor:
Swati Palit Deb, Ross B. Mikkelsen, Christopher S. Rabender, Sumitra Deb, Catherine A. Vaughan, Shilpa Singh
Publikováno v:
JCI Insight. 4
Depletion of epithelial cells after lung injury prompts proliferation and epithelial mesenchymal transition (EMT) of progenitor cells, and this repopulates the lost epithelial layer. To investigate the cell proliferative function of human oncoprotein
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3eb375be87fee72eaf212157588c1c57
https://doi.org/10.1172/jci.insight.128194
https://doi.org/10.1172/jci.insight.128194
Publikováno v:
Oncotarget
Gain-of-function mutant p53 is thought to induce gene expression in part by binding transcription factors bound to promoters for genes that mediate oncogenesis. We investigated the mechanism of mutant p53 binding by mapping the human genomic binding
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7216c48fcb34f17ba84cd35a9f4ecd55
http://europepmc.org/articles/PMC3964217
http://europepmc.org/articles/PMC3964217
Autor:
Shilpa Singh, Swati Palit Deb, Catherine A. Vaughan, Steven R. Grossman, Sumitra Deb, Brad Windle
Publikováno v:
Molecular Oncology
Gain-of-function (GOF) mutants of p53 upregulate genes implicated in cell proliferation and oncogenesis. Here, we report that GOF p53 induces tumorigenicity through simultaneous activation of key oncogenic pathways including those controlling putativ
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1e915aa1b5588994bd1644c199d7d880
https://pubmed.ncbi.nlm.nih.gov/28423230
https://pubmed.ncbi.nlm.nih.gov/28423230
Autor:
Steven R. Grossman, Shilpa Singh, Brad Windle, Sumitra Deb, Catherine A. Vaughan, Rebecca Frum, Nitai D. Mukhopadhyay, Swati Palit Deb
Publikováno v:
Nucleic Acids Research
Conventional paradigm ascribes the cell proliferative function of the human oncoprotein mouse double minute2 (MDM2) primarily to its ability to degrade p53. Here we report that in the absence of p53, MDM2 induces replication stress eliciting an early
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fd383ea04e3dafa5df77ae27a1356bc4
https://doi.org/10.1093/nar/gkt944
https://doi.org/10.1093/nar/gkt944
Autor:
Brad Windle, Catherine A. Vaughan, Isabella Pearsall, Swati Palit Deb, Sumitra Deb, Steven R. Grossman, Shilpa Singh, W. Andrew Yeudall
Publikováno v:
Oncotarget
Human lung cancers harboring gain-of-function (GOF) p53 alleles express higher levels of the epidermal growth factor receptor (EGFR). We demonstrate that a number of GOF p53 alleles directly upregulate EGFR. Knock-down of p53 in lung cancer cells low
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5e5abe746746a46a2f54f02284ca1c12
https://pubmed.ncbi.nlm.nih.gov/26820293
https://pubmed.ncbi.nlm.nih.gov/26820293
Autor:
Swati Palit Deb, Isabella Pearsall, Brad Windle, Sumitra Deb, Catherine A. Vaughan, Shilpa Singh, Andrew Yeudall, Rebecca Frum
Publikováno v:
Biochemical and Biophysical Research Communications. 428:6-10
p53 mutations are mostly single amino acid changes resulting in expression of a stable mutant protein with “gain of function” (GOF) activity having a dominant oncogenic role rather than simple loss of function of wild-type p53. Knock-down of muta
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::446894de04b6945f75be3463c2ab7ec1
https://doi.org/10.1016/j.bbrc.2012.09.029
https://doi.org/10.1016/j.bbrc.2012.09.029
Publikováno v:
Archives of Biochemistry and Biophysics. 512:52-60
The p53 gene is one of the most frequently mutated genes in human cancer. Some p53 mutations impart additional functions that promote oncogenesis. To investigate how these p53 mutants function, a proteomic analysis was performed. The protein, translo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::246bee990699512fa5323577cbc1a794
https://doi.org/10.1016/j.abb.2011.05.005
https://doi.org/10.1016/j.abb.2011.05.005