ReviewCancer science2017
Novel molecular mechanism of cellular transformation by a mutant molecular chaperone in myeloproliferative neoplasms.
Review in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Expression properties, structural features and functional analysis of CALR E381A in MPN patients.American journal of translational research · 2023Article
- Hippo pathway-related genes expression is deregulated in myeloproliferative neoplasms.Medical oncology (Northwood, London, England) · 2022Article
- Study of CALR, MPL, and c-kit Gene Mutations in Thai Patients with JAK2 V617F Negative Myeloproliferative Neoplasms.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- ERp57/PDIA3: new insight.Cellular & molecular biology letters · 2022Review
- MPL overexpression induces a high level of mutant-CALR/MPL complex: a novel mechanism of ruxolitinib resistance in myeloproliferative neoplasms with CALR mutations.International journal of hematology · 2021Article
- Unfolding the Role of Calreticulin in Myeloproliferative Neoplasm Pathogenesis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Review
- Homomultimerization of mutant calreticulin is a prerequisite for MPL binding and activation.Leukemia · 2019Article
- Article
- Tumor-associated calreticulin variants functionally compromise the peptide loading complex and impair its recruitment of MHC-I.The Journal of biological chemistry · 2018Article
- Novel molecular mechanism of cellular transformation by a mutant molecular chaperone in myeloproliferative neoplasms.Cancer science · 2017Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulation of the cytokine-receptor signaling pathway plays a significant role in tumorigenesis. Such deregulation is frequently caused by alterations in the genes involved in the signaling pathway. At the end of 2013, recurrent somatic mutations in the calreticulin (CALR) gene that encodes a molecular chaperone were identified in a subset of patients with Philadelphia-chromosome negative myeloproliferative neoplasms (MPN). The present review focuses on the role of CALR mutations in the oncogenic transformations observed in MPN. All the CALR mutations were found to generate a + 1 frameshift in the reading frame on exon 9, which encodes the carboxy (C)-terminus end of CALR, and thus conferred a common mutant-specific sequence in all the CALR mutants. The mutant CALR (but not the wild-type) constitutively activates the thrombopoietin (TPO) receptor, myeloproliferative leukemia protein (MPL), even in the absence of TPO to induce cellular transformation. Preferential interaction between the mutant CALR and MPL is achieved by a presumptive conformational change induced by the mutant-specific C-terminus domain, which allows N-domain binding to MPL. Even though mutant CALR is expressed on the cell surface and is secreted out of cells, it only presents autocrine capacity for MPL activation. These findings define a novel molecular mechanism by which the mutant molecular chaperone constitutively activates the cytokine receptor to induce cellular transformation.
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