Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P17931 (
galectin-3
)
2,860
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cellular stress response contributes to epithelial defense in adaptation to environment changes. Galectins play a pivotal role in the regulation of this response in malignant cells. However, precise underlying mechanisms are largely unknown. Here we demonstrate that
Galectin-3
, a pro and anti-apoptotic lectin, is required for setting up a correct cellular response to stress by orchestrating several effects. First,
Galectin-3
constitutes a key post-transcriptional regulator of stress-related mRNA regulons coordinating the cell metabolism, the mTORC1 complex or the unfolded protein response (UPR). Moreover, we demonstrated the presence of
Galectin-3
with mitochondria-associated membranes (MAM), and its interaction with proteins located at the ER or mitochondrial membranes. There
Galectin-3
prevents the activation and recruitment at the mitochondria of the regulator of mitochondria fission DRP-1. Accordingly, loss of
Galectin-3
impairs mitochondrial morphology, with more fragmented and round mitochondria, and dynamics both in normal and cancer epithelial cells in basal conditions. Importantly,
Galectin-3
deficient cells also display changes of the activity of the mitochondrial respiratory chain complexes, of the mTORC1/S6RP/4EBP1 translation pathway and reactive oxygen species levels. Regarding the ER,
Galectin-3
did not modify the activities of the 3 branches of the UPR in basal conditions. However,
Galectin-3
favours an adaptative UPR following ER stress induction by
Thapsigargin
treatment. Altogether, at the ER-mitochondria interface,
Galectin-3
coordinates the functioning of the ER and mitochondria, preserves the integrity of mitochondrial network and modulates the ER stress response.
...
PMID:Galectin-3 modulates epithelial cell adaptation to stress at the ER-mitochondria interface. 3239 81