Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/142359
Title: Dynamics of BCL-2 family of proteins in early pancreatic progenitors and β-cells
Authors: Loo, Larry Sai Weng
Keywords: Science::Biological sciences
Issue Date: 2020
Publisher: Nanyang Technological University
Abstract: BCL-2 family proteins play an important role in the regulation of cell survival and death. However, there are also certain members that exhibit tissue- and developmental stage-specific expression and function. Here, I report a unique reciprocal relationship between BCL-xL (not BCL2) and BAK during early human pancreatic differentiation. The association of BCL-xL but not BCL2 with BAK has also been reported to keep apoptosis in check, albeit not specifically during pancreatic development. This is consistent with our findings that the compensatory increase in BCL2 protein expression upon BCL-xL inhibition with WEHI-539 is insufficient to curb the BAK mediated increase in cleaved caspase 3 and the triggering of the caspase cascade. I also found that the downregulation of BCL2L1/BCL-xL expression and function resulted in a decrease in early pancreatic gene and protein expression. However, BCL-xL is known to be dispensable during rodent beta cell development but rather is important for protection against apoptotic stimuli in mature beta cells (Carrington et al., 2009). Therefore, I propose that BCL-xL might be indirectly involved in human pancreatic specification that is ultimately crucial for proper beta cell function.
URI: https://hdl.handle.net/10356/142359
Rights: This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0).
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Theses

Files in This Item:
File Description SizeFormat 
LL PhD Thesis 28062020 (Submit to DR NTU).pdf4.72 MBAdobe PDFView/Open

Google ScholarTM

Check

Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.