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Evaluating Autophagy Levels in Two Different Pancreatic Cell Models Using LC3 Immunofluorescence
Published on: April 28, 2023
Induction of the autophagy-associated gene MAP1S via PU.1 supports APL differentiation
Aladin Haimovici1, Daniel Brigger1, Bruce E Torbett2
1Division of Experimental Pathology, Institute of Pathology, University of Bern, Switzerland; Graduate School for Cellular and Biomedical Sciences, University of Bern, Switzerland.
Abstract:
The PU.1 transcription factor is essential for myeloid development. We investigated if the microtubule-associated protein 1S (MAP1S) is a novel PU.1 target with a link to autophagy, a cellular recycling pathway. Comparable to PU.1, MAP1S expression was significantly repressed in primary AML blasts as compared to mature neutrophils. Accordingly, MAP1S expression was induced during neutrophil differentiation of CD34(+) progenitor and APL cells. Moreover, PU.1 bound to the MAP1S promoter and induced MAP1S expression during APL differentiation. Inhibiting MAP1S resulted in aberrant neutrophil differentiation and autophagy. Taken together, our findings implicate the PU.1-regulated MAP1S gene in neutrophil differentiation and autophagy control.
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