Version 1
: Received: 17 June 2020 / Approved: 21 June 2020 / Online: 21 June 2020 (14:55:19 CEST)
Version 2
: Received: 18 October 2020 / Approved: 19 October 2020 / Online: 19 October 2020 (16:04:27 CEST)
How to cite:
Aigha, I.I.; Abdelalim, E.M. NKX6.1 Transcription Factor: A Crucial Regulator of Pancreatic β-Cell Development, Identity, and Proliferation. Preprints2020, 2020060277 (doi: 10.20944/preprints202006.0277.v1).
Aigha, I.I.; Abdelalim, E.M. NKX6.1 Transcription Factor: A Crucial Regulator of Pancreatic β-Cell Development, Identity, and Proliferation. Preprints 2020, 2020060277 (doi: 10.20944/preprints202006.0277.v1).
Cite as:
Aigha, I.I.; Abdelalim, E.M. NKX6.1 Transcription Factor: A Crucial Regulator of Pancreatic β-Cell Development, Identity, and Proliferation. Preprints2020, 2020060277 (doi: 10.20944/preprints202006.0277.v1).
Aigha, I.I.; Abdelalim, E.M. NKX6.1 Transcription Factor: A Crucial Regulator of Pancreatic β-Cell Development, Identity, and Proliferation. Preprints 2020, 2020060277 (doi: 10.20944/preprints202006.0277.v1).
Abstract
Understanding the biology underlying the mechanisms and pathways regulating pancreatic β-cell development is necessary to understand the pathology of diabetes mellitus (DM), which is characterized by the progressive reduction in insulin producing β-cell mass. Pluripotent stem cells (PSCs) can potentially offer an unlimited supply of functional β-cells for cellular therapy and disease modeling of DM. Homeobox protein NKX6.1 is a transcription factor (TF) that plays a critical role in pancreatic β-cell function and proliferation. In human pancreatic islet, NKX6.1 expression is exclusive toβ-cells and is undetectable in other islet cells. Several reports showed that activation of NKX6.1 in PSC-derived pancreatic progenitors (MPCs), expressing PDX1 (PDX1+/NKX6.1+), warrants their future commitment to monohormonal β-cells. However, further differentiation of MPCs lacking NKX6.1 expression (PDX1+/NKX6.1-) results in an undesirable generation of non-functional polyhormonal β-cells. The importance of NKX6.1 as a crucial regulator in MPC specification into functional β-cells directs attentions to further investigating its mechanism and enhancing NKX6.1 expression as a mean to increase β-cell function and mass. Here, we shed light on the role of NKX6.1 during pancreatic β-cell development and in directing the MPCs to functional monohormonal lineage. Furthermore, we address the transcriptional mechanisms and targets of NKX6.1 as well as its association with diabetes.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
