Thomas E. Ahlborn
United States Department of Veterans Affairs
6 Papers
89 Citations
Thomas E. Ahlborn is an academic researcher from United States Department of Veterans Affairs. The author has contributed to research in topics: Oncostatin M & Promoter. The author has an hindex of 6, co-authored 6 publications.
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Papers
Induction of low density lipoprotein receptor (LDLR) transcription by oncostatin M is mediated by the extracellular signal-regulated kinase signaling pathway and the repeat 3 element of the LDLR promoter.
TL;DR: The results demonstrate that the mitogen-activated protein kinase MEK/ERK cascade is the essential signaling pathway by which OM activates LDLR gene transcription and provide the first evidence that the repeat 3 element is a new downstream target of ERK activation.
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Identification of a novel sterol-independent regulatory element in the human low density lipoprotein receptor promoter.
TL;DR: This study identifies, for the first time, acis-acting regulatory element in the LDLR promoter that is responsible for sterol-independent regulation of LDLR transcription.
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Oncostatin M-induced growth inhibition and morphological changes of MDA-MB231 breast cancer cells are abolished by blocking the MEK/ERK signaling pathway.
TL;DR: It is shown that OM rapidly activates the extracellular signal‐regulated kinase (ERK) and the signal transducer and activator of transcription (STAT) 1 and 3 in both cell lines and demonstrates that the growth‐inhibitory activity of OM can be mediated by different signaling pathways in a cell line‐specific manner.
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Identification of Egr1 as the oncostatin M-induced transcription activator that binds to sterol-independent regulatory element of human LDL receptor promoter
TL;DR: The studies clearly demonstrate that Egr1 is the OM-induced transcription factor that binds to the SIRE sequence of the LDLR promoter and suggest that EGr1 may have a functional role in OM- induced upregulation of LDLR transcription through interaction with other SIRE binding proteins such as c/EBPβ or CREB.
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•Journal Article
The Expression of p53 Tumor Suppressor Gene in Breast Cancer Cells Is Down-Regulated by Cytokine Oncostatin M
TL;DR: The data suggest that p53 expression in breast cancer cells is down-regulated during the differentiation process, which suggests a transcriptional regulatory mechanism.
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