N
Nicole Schreiber-Agus
Researcher at Albert Einstein College of Medicine
Publications - 55
Citations - 5945
Nicole Schreiber-Agus is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Gene & Transcription factor. The author has an hindex of 30, co-authored 55 publications receiving 5767 citations. Previous affiliations of Nicole Schreiber-Agus include Yeshiva University & Jacobi Medical Center.
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Journal ArticleDOI
The Ink4a Tumor Suppressor Gene Product, p19Arf, Interacts with MDM2 and Neutralizes MDM2's Inhibition of p53
Jason H. Pomerantz,Nicole Schreiber-Agus,Nanette J. Liégeois,Adam Silverman,Leila Alland,Lynda Chin,Jason Potes,Ken Chen,Irene Orlow,Han Woong Lee,Han Woong Lee,Carlos Cordon-Cardo,Ronald A. DePinho +12 more
TL;DR: It is shown that p19Arf potently suppresses oncogenic transformation in primary cells and that this function is abrogated when p53 is neutralized by viral oncoproteins and dominant-negative mutants but not by the p53 antagonist MDM2.
Journal ArticleDOI
Role for N-CoR and histone deacetylase in Sin3-mediated transcriptional repression
Lelia Alland,Rebecca Muhle,Harry Hou,Jason Potes,Lynda Chin,Nicole Schreiber-Agus,Ronald A. DePinho +6 more
TL;DR: The identification of the nuclear receptor co-repressor (N-CoR) and histone deacetylase (HD1) provides a basis for Mxi1/Sin3-induced transcriptional repression and tumour suppression.
Journal ArticleDOI
An amino-terminal domain of Mxi1 mediates anti-myc oncogenic activity and interacts with a homolog of the Yeast Transcriptional Repressor SIN3
Nicole Schreiber-Agus,Lynda Chin,Ken Chen,Richard Torres,Govinda Rao,Peter Guida,Arthur I. Skoultchi,Ronald A. DePinho +7 more
TL;DR: Findings provide a mechanistic basis for the antagonistic actions of Mxi1 on Myc activity that appears to be mediated in part through the recruitment of a putative transcriptional repressor.
Journal ArticleDOI
Inhibition of experimental liver cirrhosis in mice by telomerase gene delivery.
TL;DR: It is indicated that telomere dysfunction contributes to chronic diseases of continual cellular loss-replacement and the evaluation of "telomerase therapy" for such diseases is encouraged.
Book ChapterDOI
myc family oncogenes in the development of normal and neoplastic cells.
TL;DR: Myc family oncoproteins are localized to the nucleus, and they possess significant homology to known sequence-specific transcription factors and for differentiation factors, thereby suggesting that myc -encoded oncoproteinins may serve to regulate specific gene expression during growth and differentiation.