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Erin J. Cram

Researcher at Northeastern University

Publications -  70
Citations -  1537

Erin J. Cram is an academic researcher from Northeastern University. The author has contributed to research in topics: Caenorhabditis elegans & Distal tip cell migration. The author has an hindex of 17, co-authored 65 publications receiving 1319 citations. Previous affiliations of Erin J. Cram include University of North Carolina at Chapel Hill & Princeton University.

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Journal Article

Indole-3-carbinol and tamoxifen cooperate to arrest the cell cycle of MCF-7 human breast cancer cells.

TL;DR: Results demonstrate that I3C and tamoxifen work through different signal transduction pathways to suppress the growth of human breast cancer cells and may, therefore, represent a potential combinatorial therapy for estrogen-responsive breast cancer.
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Glucocorticoids Stimulate p21 Gene Expression by Targeting Multiple Transcriptional Elements within a Steroid Responsive Region of the p21 waf1/cip1 Promoter in Rat Hepatoma Cells

TL;DR: The results have established a direct transcriptional link between glucocorticoid receptor signaling and the regulated promoter activity of a CDK inhibitor gene that is involved in the cell cycle arrest of hepatoma cells.
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Role of the CCAAT/Enhancer Binding Protein-α Transcription Factor in the Glucocorticoid Stimulation of p21 waf1/cip1 Gene Promoter Activity in Growth-arrested Rat Hepatoma Cells *

TL;DR: A functional link is established between the glucocorticoid receptor signaling pathway that mediates a G1 cell cycle arrest of rat hepatoma cells and the transcriptional control of p21 by a cascade that requires the steroid induction of C/EBPα gene expression.
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Talin loss-of-function uncovers roles in cell contractility and migration in C. elegans.

TL;DR: In vivo analyses show that talin is required not only for strong adhesion and cytoskeletal organization by contractile cells, but also for dynamic regulation of integrin signals during cell migration.
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Indole-3-carbinol Inhibits CDK6 Expression in Human MCF-7 Breast Cancer Cells by Disrupting Sp1 Transcription Factor Interactions with a Composite Element in the CDK6 Gene Promoter

TL;DR: The results suggest that I3C down-regulatesCDK6 transcription by targeting Sp1 at a composite DNA site in the CDK6 promoter.