Control of macroautophagy by calcium, calmodulin-dependent kinase kinase-beta, and Bcl-2.

By M. Høyer-Hansen, L. Bastholm, P. Szyniarowski, M. Campanella, G. Szabadkai, T. Farkas, K. Bianchi, Nicole Fehrenbacher, F. Elling, R. Rizzuto and 2 more. Molecules and Cells, 2007

1,137 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/8709902de68a28924084a864a4b90fe9a0e90072

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

In Epidemiology

In Physiology

Citations in the corpus

Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “An increase in calcium, as occurs during ischemia, has been shown to increase autophagy (107).”
Calcium and apoptosis: ER-mitochondria Ca2+ transfer in the control of apoptosis (2008, background): “Hoyer-Hansen et al. (2007) demonstrated recently that various Ca2þ mobilizing stimuli, such as vitamin D3 compounds, ATP, thapsigargin and ionomycin, by inducing an increase in [Ca2þ ]c, activate the Ca 2þ /calmodulindependent protein kinase-kinase (CaMKK) and consequently inhibit mTOR (mammalian…”
New insights into the interplay between autophagy, gut microbiota and inflammatory responses in IBD (2019, background): “In response to extended ER stress, unfolded protein response activation induces Ca release from the ER, which in turn activates the key regulator of autophagy AMPK (AMP-activated protein kinase) [40].”
Linking of autophagy to ubiquitin-proteasome system is important for the regulation of endoplasmic reticulum stress and cell viability. (2007, background): “autophagy induction downstream of IRE1 signaling, our studies do not exclude the possibility that XBP-1 can participate in autophagy induced through other means and do not exclude simultaneous participation of other mechanisms in parallel with the JNK signaling, in particular the calcium/calmodulin-”
Connecting endoplasmic reticulum stress to autophagy by unfolded protein response and calcium (2007, neutral): “In addition to activating the UPR by the pathways discussed above, ER-stress leads to a release of Ca2þ from the ER into the cytosol, which, in turn, can activate various kinases and proteases possibly involved in autophagy signaling.(24,38,39)”