The endoplasmic reticulum and mitochondria continuously transfer information to sustain intracellular homeostasis. This transfer is achieved by physical contact between the two organelles. The ...

Human, animal, and cellular studies have revealed that metabolic alterations can perturb mitochondria–ER contact sites. In this section, we review the observations that document the impact of altered ...

Interestingly, mitochondria-ER tethering suppresses mitophagy and parkin/PINK1-dependent mechanism regulates the destruction of mitochondria-ER contact sites by catalyzing a rapid burst of Mfn2 ...

The mitochondria-endoplasmic reticulum contact sites (MERCS) also play a pivotal role in facilitating Ca 2+ transfer. Dysregulation at any level, such as excessive uptake or impaired efflux ...

The S1R is a protein enriched at the endoplasmic reticulum (ER)-mitochondria interface and vital to multiple cellular mechanisms, including mitochondrial function and the ER stress response. By ...

The mitochondria-endoplasmic reticulum contact sites (MERCS) also play a pivotal role in facilitating Ca 2+ transfer. Dysregulation at any level, such as excessive uptake or impaired efflux, leads to ...