Search Results - "LEWALLEN, Michelle E"
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MUC1 mucin stabilizes and activates hypoxia-inducible factor 1 alpha to regulate metabolism in pancreatic cancer
Published in Proceedings of the National Academy of Sciences - PNAS (21-08-2012)“…Aberrant glucose metabolism is one of the hallmarks of cancer that facilitates cancer cell survival and proliferation. Here, we demonstrate that MUC1, a large,…”
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Cyclin-Dependent Kinase 5 Is Amplified and Overexpressed in Pancreatic Cancer and Activated by Mutant K-Ras
Published in Clinical cancer research (01-10-2011)“…To evaluate the nature of cyclin-dependent kinase 5 (CDK5) hyperactivity in pancreatic cancer progression. We used genetic, biochemical, and molecular biology…”
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MUC1 regulates expression of multiple microRNAs involved in pancreatic tumor progression, including the miR-200c/141 cluster
Published in PloS one (15-10-2013)“…MUC1 is a transmembrane glycoprotein that modulates transcription via its cytoplasmic domain. We evaluated the capacity of MUC1 to regulate the global…”
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The glycoprotein mucin‐1 negatively regulates GalNAc transferase 5 expression in pancreatic cancer
Published in FEBS letters (01-10-2019)“…Aberrant expression of the glycoprotein mucin‐1 (MUC1) has been associated with pancreatic cancer progression and metastasis as a result of mediating the…”
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MUC1 Negatively Regulates GalNAc Transferase 5 Expression in Pancreatic Cancer
Published in FEBS letters (21-07-2019)“…Aberrant expression of MUC1 glycoprotein has been associated with pancreatic cancer (PC) progression and metastasis and mediates oncogenic transcriptional…”
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Abstract 2308: MUC1 modulation of E-cadherin through miR-200c and ZEB1
Published in Cancer research (Chicago, Ill.) (15-04-2012)“…MUC1, a cell-surface glycoprotein implicated in tumorigenesis and metastasis, has a cytoplasmic tail (MUC1.CT) that is phosphorylated by different receptor…”
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Cyclin Dependent Kinase 5 is amplified and over-expressed in pancreatic cancer and activated by mutant K-Ras
Published in Clinical cancer research (08-08-2011)Get full text
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