Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-β

By T. Nakagawa, Hong Zhu, N. Morishima, En Li, Jin Xu, B. Yankner, Junying Yuan. Nature, 2000

3,419 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f629385a478ade0206fe13db93e42d94340a1a3a

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

1. R. Kaufman
2. G. Hotamışlıgil
3. D. Ron
4. J. Malhotra
5. H. Harding
6. C. Hetz
7. Afshin Samali
8. A. Gorman

In Epidemiology

1. R. Kaufman
2. Guido Kroemer
3. N. Mizushima
4. J. Malhotra
5. Beth Levine
6. D. Klionsky
7. D. Ron
8. G. Hotamışlıgil

In Molecular Biology

1. R. Kaufman
2. G. Hotamışlıgil
3. D. Ron
4. Guido Kroemer
5. Jerry M. Adams
6. J. Malhotra
7. Junying Yuan
8. H. Harding

Citations in the corpus

• Mechanisms of pre‐apoptotic calreticulin exposure in immunogenic cell death (2009, background): “Unexpectedly, neither the ER stress- elicited caspase, caspase-12 (Nakagawa et al, 2000), nor the most common effector caspases-3 or -7 were involved in CRT/ERp57 exposure, because casp12 / or casp3 / casp7 / mouse embryonic fibroblasts (MEFs) maintained the capacity to expose CRT/ERp57 in a…”
• Doxorubicin-induced cardiomyopathy: from molecular mechanisms to therapeutic strategies. (2012, neutral): “reticulum, namely calpain dysregulation [75].”
• Caspases in Cell Death, Inflammation, and Gasdermin-Induced Pyroptosis (2020, background): “Caspase-12 seems to mediate ER-stress-induced apoptosis but is dispensable for apoptosis induced by classical stimuli (97, 99, 100).”
• Caspase functions in cell death and disease. (2013, background): “…death stimuli; thus, caspase-12 mediates an ER-specific apoptosis pathway; show an enhanced bacterial clearance and are more resistant to sepsis Nakagawa et al. 2000; Saleh et al. 2006 Caspase-14 Develop normally and are fertile; their long-term survival was indistinguishable from that of…”
• IRE1-mediated unconventional mRNA splicing and S2P-mediated ATF6 cleavage merge to regulate XBP1 in signaling the unfolded protein response. (2002, background): “In addition, if adaptation is not sufficient, apoptosis is activated, possibly mediated by the c-Jun N-terminal protein kinase JNK, and activation of caspases 7 and 12 (Chandler et al. 1998; Nakagawa et al. 2000; Urano et al. 2000a).”
• The immunology of sepsis (2008, background): “While the apoptotic pathways described above would be considered to act through the classical caspase-8- and -9-dependent pathways, recent evidence has been produced in favour of a role for another caspase family member in susceptibility to sepsis, caspase-12, which has been implicated both as a med”