Journal article
Ronan Russell, Phichitpol P. Carnese, Thomas G. Hennings, E. Walker, H. Russ, Jennifer S. Liu, Simone Giacometti, R. Stein, M. Hebrok
Nature Communications, 2020
Nature Communications, 2020
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APA
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Russell, R., Carnese, P. P., Hennings, T. G., Walker, E., Russ, H., Liu, J. S., … Hebrok, M. (2020). Loss of the transcription factor MAFB limits β-cell derivation from human PSCs. Nature Communications.
Chicago/Turabian
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Russell, Ronan, Phichitpol P. Carnese, Thomas G. Hennings, E. Walker, H. Russ, Jennifer S. Liu, Simone Giacometti, R. Stein, and M. Hebrok. “Loss of the Transcription Factor MAFB Limits β-Cell Derivation from Human PSCs.” Nature Communications (2020).
MLA
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Russell, Ronan, et al. “Loss of the Transcription Factor MAFB Limits β-Cell Derivation from Human PSCs.” Nature Communications, 2020.
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@article{ronan2020a,
title = {Loss of the transcription factor MAFB limits β-cell derivation from human PSCs},
year = {2020},
journal = {Nature Communications},
author = {Russell, Ronan and Carnese, Phichitpol P. and Hennings, Thomas G. and Walker, E. and Russ, H. and Liu, Jennifer S. and Giacometti, Simone and Stein, R. and Hebrok, M.}
}
Abstract
Next generation sequencing studies have highlighted discrepancies in β-cells which exist between mice and men. Numerous reports have identified MAF BZIP Transcription Factor B (MAFB) to be present in human β-cells postnatally, while its expression is restricted to embryonic and neo-natal β-cells in mice. Using CRISPR/Cas9-mediated gene editing, coupled with endocrine cell differentiation strategies, we dissect the contribution of MAFB to β-cell development and function specifically in humans. Here we report that MAFB knockout hPSCs have normal pancreatic differentiation capacity up to the progenitor stage, but favor somatostatin- and pancreatic polypeptide–positive cells at the expense of insulin- and glucagon-producing cells during endocrine cell development. Our results describe a requirement for MAFB late in the human pancreatic developmental program and identify it as a distinguishing transcription factor within islet cell subtype specification. We propose that hPSCs represent a powerful tool to model human pancreatic endocrine development and associated disease pathophysiology. The MAF bZIP transcription factor B (MAFB) is present in postnatal human beta cells but its role is unclear. Here, the authors show that MAFB regulates endocrine pancreatic cell fate specification.