How does TGM2 mechanistically regulate ER-mitochondria contact sites in neuronal cells?

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Description

The abstract identifies TGM2 as a key regulator of ER-mitochondria contacts affecting calcium homeostasis, but the specific molecular mechanisms by which TGM2 modulates these contact sites remain unclear. Understanding this mechanism is crucial for developing targeted therapies for diabetes-associated neurodegeneration.

Gap type: unexplained_observation Source paper: Urolithin A suppresses high glucose-induced neuronal amyloidogenesis by modulating TGM2-dependent ER-mitochondria contacts and calcium homeostasis. (2021, Cell Death Differ, PMID:32704090)

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