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Eric G. Neilson

Researcher at Northwestern University

Publications -  247
Citations -  31746

Eric G. Neilson is an academic researcher from Northwestern University. The author has contributed to research in topics: Antigen & Immune system. The author has an hindex of 73, co-authored 247 publications receiving 29759 citations. Previous affiliations of Eric G. Neilson include University of Kansas & University of Michigan.

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TGF-ß Signaling in Fibroblasts Modulates the Oncogenic Potential of Adjacent Epithelia

TL;DR: TGF-β signaling in fibroblasts modulates the growth and oncogenic potential of adjacent epithelia in selected tissues and is associated with intraepithelial neoplasia in prostate and invasive squamous cell carcinoma of the forestomach.
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Identification and characterization of a fibroblast marker: FSP1.

TL;DR: Experiments in which the in vitro overexpression of FSP1 cDNA in tubular epithelium is accompanied by conversion to a mesenchymal phenotype are observed, as characterized by a more stellate and elongated fibroblast- like appearance, a reduction in cytokeratin, and new expression of vimentin.
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Heart repair by reprogramming non-myocytes with cardiac transcription factors

TL;DR: It is shown that four transcription factors, GATA4, HAND2, MEF2C and TBX5, can cooperatively reprogram adult mouse tail-tip and cardiac fibroblasts into beating cardiac-like myocytes in vitro and suggest a strategy for cardiac repair through reprogramming fibro Blasts resident in the heart with cardiogenic transcription factors or other molecules.
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Alport's Syndrome, Goodpasture's Syndrome, and Type IV Collagen

TL;DR: In this article, the authors have shown that mutations in genes corresponding to the building blocks of type IV collagen cause Alport's syndrome, whereas autoantibodies against structures that are usually hidden in the recesses of collagen IV cause Goodpasture's syndrome.
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Mechanisms of Tubulointerstitial Fibrosis

TL;DR: In combination with traditional angiotensin converting enzyme inhibitors, newly identified cytokines may eventually form the basis for new therapeutic strategies aimed at inhibiting the progression of renal disease.