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Patricia C. Cogswell

Researcher at University of North Carolina at Chapel Hill

Publications -  29
Citations -  7099

Patricia C. Cogswell is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Regulation of gene expression & Transcription factor. The author has an hindex of 27, co-authored 29 publications receiving 6849 citations.

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Role of Transcriptional Activation of IκBα in Mediation of Immunosuppression by Glucocorticoids

TL;DR: It is shown that the synthetic glucocorticoid dexamethasone induces the transcription of the IκBα gene, which results in an increased rate of Iκbα protein synthesis, which is predicted to markedly decrease cytokine secretion and thus effectively block the activation of the immune system.
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axl, a transforming gene isolated from primary human myeloid leukemia cells, encodes a novel receptor tyrosine kinase.

TL;DR: Using a sensitive transfection-tumorigenicity assay, a novel transforming gene from the DNA of two patients with chronic myelogenous leukemia is isolated and sequence analysis indicates that the product of this gene, axl, is a receptor tyrosine kinase.
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Requirement of NF-κB Activation to Suppress p53-Independent Apoptosis Induced by Oncogenic Ras

TL;DR: The results provide an explanation for the requirement of NF-kappaB for Ras-mediated oncogenesis and provide evidence that Ras-transformed cells are susceptible to apoptosis even if they do not express the p53 tumor-suppressor gene product.
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Akt-dependent regulation of NF-κB is controlled by mTOR and Raptor in association with IKK

TL;DR: It is shown here that mTOR downstream from Akt controls NFB activity in PTEN-null/inactive prostate cancer cells via interaction with and stimulation of IKK, and the mTOR-associated protein Raptor is required for the ability of Akt to induce N FB activity.
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Functional and physical associations between NF-kappa B and C/EBP family members: a Rel domain-bZIP interaction.

TL;DR: These studies demonstrate that NF-kappa B augments gene expression mediated by a multimerized c-fos serum response element in the presence of C/EBP.