Secreted calreticulin mutants subvert anticancer immunosurveillance.
Immunogenic cell death
PD-1 blockade
retention using selective hooks
Journal
Oncoimmunology
ISSN: 2162-4011
Titre abrégé: Oncoimmunology
Pays: United States
ID NLM: 101570526
Informations de publication
Date de publication:
2020
2020
Historique:
received:
09
12
2019
accepted:
19
12
2019
entrez:
1
2
2020
pubmed:
1
2
2020
medline:
1
2
2020
Statut:
epublish
Résumé
Mutations of the gene coding for calreticulin (CALR) that cause the loss of the C-terminal KDEL motif abolish its retention in the endoplasmic reticulum and cause CALR to be secreted from cells. Specific CALR mutants bearing a novel C-terminus can precipitate the manifestation of myeloproliferative diseases via the autocrine activation of the thrombopoietin receptor. We recently employed the retention using selective hooks (RUSH) technology to monitor CALR trafficking and demonstrated the secretion of C-terminally truncated variants of CALR
Identifiants
pubmed: 32002304
doi: 10.1080/2162402X.2019.1708126
pii: 1708126
pmc: PMC6959454
doi:
Substances chimiques
Calreticulin
0
Types de publication
Editorial
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
1708126Informations de copyright
© 2019 The Author(s). Published with license by Taylor & Francis Group, LLC.
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