Title : Restoration of the immunogenicity of cisplatin-induced cancer cell death by endoplasmic reticulum stress.

Pub. Date : 2011 Mar 10

PMID : 21151176






6 Functional Relationships(s)
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Protein Name
Organism
1 This failure to induce immunogenic cell death can be attributed to CDDP"s incapacity to elicit the translocation of calreticulin (CRT) from the lumen of the endoplasmic reticulum (ER) to the cell surface. Cisplatin calreticulin Homo sapiens
2 This failure to induce immunogenic cell death can be attributed to CDDP"s incapacity to elicit the translocation of calreticulin (CRT) from the lumen of the endoplasmic reticulum (ER) to the cell surface. Cisplatin calreticulin Homo sapiens
3 Using a screening method that monitors the voyage of CRT from the ER lumen to the cell surface, we identified thapsigargin (THAPS), an inhibitor of the sarco/ER Ca(2+)-ATPase as a molecule that on its own does not stimulate CRT exposure, yet endows CDDP with the capacity to do so. Cisplatin calreticulin Homo sapiens
4 The combination of ER stress inducers (such as THAPS or tunicamycin) and CDDP effectively induced the translocation of CRT to the plasma membrane, as well as immunogenic cell death, although ER stress or CDDP alone was insufficient to induce CRT exposure and immunogenic cell death. Cisplatin calreticulin Homo sapiens
5 The combination of ER stress inducers (such as THAPS or tunicamycin) and CDDP effectively induced the translocation of CRT to the plasma membrane, as well as immunogenic cell death, although ER stress or CDDP alone was insufficient to induce CRT exposure and immunogenic cell death. Cisplatin calreticulin Homo sapiens
6 The combination of ER stress inducers (such as THAPS or tunicamycin) and CDDP effectively induced the translocation of CRT to the plasma membrane, as well as immunogenic cell death, although ER stress or CDDP alone was insufficient to induce CRT exposure and immunogenic cell death. Cisplatin calreticulin Homo sapiens