MAM

By Teruo Hayashi, R. Rizzuto, G. Hajnóczky, T. Su. Trends in Cell Biology, 2009

764 citations recorded by the source corpus.

The physical association between the endoplasmic reticulum (ER) and mitochondria, which is known as the mitochondria-associated ER membrane (MAM), has important roles in various cellular ‘housekeeping’ functions including the non-vesicular transports of phospholipids. It has recently become clear that the MAM also enables highly efficient transmission of Ca2+ from the ER to mitochondria to stimulate oxidative metabolism and, conversely, might enable the metabolically energized mitochondria to regulate the ER Ca2+ homeostasis. Recent studies have shed light on molecular chaperones such as calnexin, calreticulin, ERp44, ERp57, grp75 and the sigma-1 receptor at the MAM, which regulate the association between the two organelles. The MAM thus integrates signal transduction with metabolic pathways to regulate the communication and functional interactions between the ER and mitochondrion.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/96d9aa57ede6d87d890e76793536efc89d100886

How researchers see this paper

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

In Cellular and Molecular Neuroscience

1. R. Rizzuto
2. Lin Tian
3. L. Looger
4. Cori Bargmann
5. J. Nunnari
6. Karl Deisseroth
7. David W. Tank

In Molecular Biology

1. A. Suomalainen
2. J. Nunnari
3. R. Rizzuto
4. L. Looger
5. Cori Bargmann
6. Afshin Samali

Citations in the corpus

• PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress (2012, background): “MFN2 / cells displayed delayed kinetics of CHOP induction (Figure 5c) and caspase-3 processing after phox-ER stress as compared with Figure 6 PERK is required to maintain ER-mitochondrial contact sites and for phox-ER stress induced relocation of mitochondria to the ER.”
• Upregulated function of mitochondria-associated ER membranes in Alzheimer disease (2012, neutral): “…, 2010; Giacomello et al , 2010), as MAM is highly enriched in the sarco-ER calcium-ATPase (de Meis et al , 2010), the sigma-1 receptor (Hayashi and Fujimoto, 2010), ryanodine receptors (RyRs) (Garcı´a-Pe´rez et al , 2008), and inositol-1,4,5-trisphosphate receptors (IP3Rs) (Hayashi et al , 2009).”
• Imaging interorganelle contacts and local calcium dynamics at the ER-mitochondrial interface (2010, neutral): “, 2009) and is required for many aspects of cell function in mammalian cells, including lipid biosynthesis, protein trafficking, and calcium signaling (Goetz and Nabi, 2006; Hayashi et al., 2009; Vance, 2003; Voelker, 2009; Wiedemann et al., 2009).”
• Mitochondria in the regulation of innate and adaptive immunity (2015, neutral): “MAM provides a mitochondrial/ER inter-organelle communication that regulates stress and metabolic signaling (Hayashi et al., 2009).”
• Genetically encoded calcium indicators for multi-color neural activity imaging and combination with optogenetics (2013, background): “Upon stimulation of Ca2+ release from the endoplasmic reticulum (ER) by addition of 10 mM caffeine, RCaMP fluorescence initially rose together with GCaMP fluorescence (Figure 5E), consistent with Ca2+ release from the ER through the mitochondrialassociated membrane (MAM) (Hayashi et al., 2009), whil”
• Mitochondria: In Sickness and in Health (2012, background): “MAMs create unique environments or platforms for the localization and activity of components that function in shared interorganellar functions, such as Ca2+ homeostasis and lipid biosynthesis (Hayashi et al., 2009; Rizzuto and Pozzan, 2006; Voelker, 2009).”