TMEM55A-mediated PI5P signalling regulates alpha cell actin depolymerisation and glucagon secretion.

ABSTRACT:

Aims/hypothesis

Diabetes is associated with the dysfunction of glucagon-producing pancreatic islet alpha cells, although the underlying mechanisms regulating glucagon secretion and alpha cell dysfunction remain unclear. While insulin secretion from pancreatic beta cells has long been known to be controlled partly by intracellular phospholipid signalling, very little is known about the role of phospholipids in glucagon secretion. Using patch-clamp electrophysiology and single-cell RNA sequencing, we previously found that expression of PIP4P2 (encoding TMEM55A, a lipid phosphatase that dephosphorylates phosphatidylinositol-4,5-bisphosphate [PIP2] to phosphatidylinositol-5-phosphate [PI5P]) correlates with alpha cell function. We hypothesise that TMEM55A is involved in glucagon secret

SUBMITTER: Liu X 

PROVIDER: S-EPMC12176968 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature