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A new, inflammatory function for an ‘orphan’ cell death protein
BCL-G, a hitherto ‘orphan’ member of the BCL-2 protein family of cell death regulators, regulates inflammatory responses and not cell death in dying intestinal epithelial cells – finds a study led by Dr Ken Nally and published recently in Cell Death & Disease.
Most diseases are connected in some way to defective regulation of cell death. The BCL-2 proteins are evolutionarily conserved sentinels of cellular stress that control mitochondrial apoptosis, a specialised form of regulated cell death. Over the past 30 years, multiple BCL-2 family members have been identified, many of which are now fully integrated into networks underpinning mitochondrial apoptosis. For some, however, an exact role in cell death signalling remains unclear. One such ‘orphan’ BCL-2 family member was BCL-G. Now, Jerzy Woznicki – a postdoctoral researcher working in Dr Ken Nally’s team – has demonstrated that BCL-G regulates chemokine secretion but not apoptosis triggered by an inflammatory stress in intestinal epithelial cells. Together with the observed changes in mucosal expression of BCL-G in inflammatory bowel disease and colorectal cancer, this study highlights a potential immunomodulatory role for BCL-G in the human gut.
Woznicki, Jerzy & Flood, Peter & Bustamante, Milan & Stamou, Panagiota & Moloney, Gerard & Fanning, Aine & Zulquernain, Syed & McCarthy, Jane & Shanahan, Fergus & Melgar, Silvia & Nally, Kenneth. (2020). Human BCL-G regulates secretion of inflammatory chemokines but is dispensable for induction of apoptosis by IFN-γ and TNF-α in intestinal epithelial cells. Cell Death & Disease. 11. 10.1038/s41419-020-2263-0.