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Alison Bamberg

Researcher at University of Colorado Denver

Publications -  5
Citations -  263

Alison Bamberg is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Myofibroblast & Apoptosis. The author has an hindex of 3, co-authored 5 publications receiving 223 citations.

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Journal ArticleDOI

Autophagy variation within a cell population determines cell fate through selective degradation of Fap-1

TL;DR: It is demonstrated that transient cell-to-cell variations in autophagy can promote either cell death or survival depending on the stimulus and cell type, and differences in autophile in a cell population determine cell fate in a stimulus- and cell-type-specific manner.
Journal ArticleDOI

Increased Cell Surface Fas Expression Is Necessary and Sufficient To Sensitize Lung Fibroblasts to Fas Ligation-Induced Apoptosis: Implications for Fibroblast Accumulation in Idiopathic Pulmonary Fibrosis

TL;DR: It is suggested that increased expression of Fas is necessary and sufficient to overcome the resistance of lung fibroblasts to Fas-induced apoptosis and that approaches aimed at increasing Fas expression by lung fibrablasts and myofibroblast may be therapeutically relevant in IPF.
Journal ArticleDOI

Protein Tyrosine Phosphatase-N13 Promotes Myofibroblast Resistance to Apoptosis in Idiopathic Pulmonary Fibrosis.

TL;DR: Findings suggest that PTPN13 mediates the resistance of human lung (myo)fibroblasts to Fas‐induced apoptosis and promotes pulmonary fibrosis in mice, and suggest that strategies aimed at interfering with PTPn13 expression or function may represent a novel strategy to reduce fibrosisIn IPF.
Patent

Compositions and methods to induce targeted apoptosis

TL;DR: In this article, compositions and methods for treating a subject having or suspected of developing a pulmonary disorder or cancer were discussed, and certain embodiments concern modulating protein tyrosine phosphatase non-receptor type 13 (PTPN13) expression and/or activity in a subject to treat uncontrolled cellular growth in the subject.