ArticleCell biology international2025
CALR Type 1-Like Mutations Increase Endoplasmic Reticulum Free Ca
Article in Cell biology international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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3 authors.
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Abstract
Calreticulin is a multifunctional protein found in the endoplasmic reticulum lumen that is important for calcium homeostasis and glycoprotein folding. Mutations in exon 9 of the CALR gene are the second most common genetic cause of myeloproliferative neoplasms. CALR-mutated megakaryocyte proliferation in myeloproliferative neoplasms involves cytokine-independent constitutive activation of JAK/STAT signaling caused by binding of mutant calreticulin to the thrombopoietin receptor. However, whether the partial or complete removal of wildtype calreticulin from the endoplasmic reticulum has additional effects on megakaryocyte biology is not clear. To explore the impact of calreticulin mutations independent of thrombopoietin receptor signaling we generated type 1-like CALR mutations in K-562 cells, which do not express the thrombopoietin receptor. We confirmed that the loss of endoplasmic reticulum-retention KDEL motif causes the majority of mutant calreticulin to be secreted from cells. The CALR mutated cells have higher endoplasmic reticulum free Ca
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