The Ca2+ concentration of the endoplasmic reticulum is a key determinant of ceramide‐induced apoptosis: significance for the molecular mechanism of Bcl‐2 action

By P. Pinton, D. Ferrari, E. Rapizzi, F. Virgilio, T. Pozzan, R. Rizzuto. EMBO Journal, 2001

629 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9203f3bf25a8b855df81d180c223f0ab8c513f3b

How researchers see this paper

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

In Immunology

1. T. Balla
2. R. Kaufman
3. M. Fuller
4. Alexei Verkhratsky

In Molecular Biology

1. R. Youle
2. M. Karbowski
3. Simon Cook
4. H. Llewelyn Roderick
5. P. Pinton
6. C. Giorgi
7. R. Rizzuto
8. T. Balla

Citations in the corpus

• Endoplasmic reticulum stress contributes to beta cell apoptosis in type 2 diabetes (2007, background): “Increased formation of ceramide is a possibility since this is implicated in beta cell lipotoxicity [5, 6], and in other cell-types ceramide has been shown to perturb ER Ca homeostasis [42].”
• Mitochondrial calcium signalling and cell death: approaches for assessing the role of mitochondrial Ca2+ uptake in apoptosis. (2006, background): “In the late 90s, studies of the propagation of the IP3 receptor (IP3R)- and ryanodine receptor (RyR)-mediated [Ca]c oscillations to the mitochondria provided the unexpected result that physiological [Ca]m transients can also trigger mitochondrial membrane permeabilization, leading to apoptotic cell ”
• Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels (2006, background): “…(the mitochondrial Ca2+ uniporter), regulates processes as diverse as aerobic metabolism (Hajnoczky et al., 1995), release of caspase cofactors (Pinton et al., 2001), and feedback control of neighboring ER or plasma membrane Ca2+ channels (Hajnoczky et al., 1999; Gilabert and Parekh, 2000).”
• Physiology and pathophysiology of the calcium store in the endoplasmic reticulum of neurons. (2005, background): “Indeed, it is evident that dramatic falls in intra-ER free Ca(2) are detrimental for the cell; however, increased [Ca(2) ]L can also be toxic (147, 511).”
• Spatial and temporal association of Bax with mitochondrial fission sites, Drp1, and Mfn2 during apoptosis (2002, background): “…has been reported to occur during apoptosis induced by a variety of unrelated stimuli (Mancini et al., 1997; Desagher and Martinou, 2000; Chen et al., 2001; Frank et al., 2001; Pinton et al., 2001) and truncated Bid induces morphological remodeling of mitochondrial cristae (Scorrano et al., 2002).”
• Imaging interorganelle contacts and local calcium dynamics at the ER-mitochondrial interface (2010, positive): “Regarding calcium, the junctions provide a site where the IP3R/ryanodine receptor (RyR)-mediated calcium oscillations are propagated locally to the mitochondria to control energy metabolism and mitochondrial apoptosis and to exert feedback effects on cytoplasmic calcium signaling (Breckenridge et al”
• Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival (2008, background): “Indeed, despite controlling many processes essential for life, Ca 2+ arising from the ER can be a potent death-inducing signa”