Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

CALR-mutated cells are vulnerable to combined inhibition of the proteasome and the endoplasmic reticulum stress response.

Leukemia - 1 Feb 2023

Jutzi Jonas S, Marneth Anna E, Jiménez-Santos María José, Hem Jessica, Guerra-Moreno Angel, Rolles Benjamin, Bhatt Shruti, Myers Samuel A, Carr Steven A, Hong Yuning, Pozdnyakova Olga, van Galen Peter, Al-Shahrour Fátima, Nam Anna S, Mullally Ann

Abstract excerpt

Cancer is driven by somatic mutations that provide a fitness advantage. While targeted therapies often focus on the mutated gene or its direct downstream effectors, imbalances brought on by cell-state alterations may also confer unique vulnerabilities. In myeloproliferative neoplasms (MPN), somatic mutations in the calreticulin (CALR) gene are disease-initiating through aberrant binding of mutant CALR to the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Calreticulin
Share to Cytoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Endoplasmic Reticulum Stress

Share to Janus Kinase 2

Share to Mutation

Share to Myeloproliferative Disorders

Share to Proteasome Endopeptidase Complex

Share to Protein Serine-Threonine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 36473980
DOI: 10.1038/s41375-022-01781-0
PMCID: PMC12413246

Genes

CALR
MPL
XBP1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

CALR-mutated cells are vulnerable to combined inhibition of the proteasome and the endoplasmic reticulum stress response.PMID 36473980Read ↗

Human gene-engineered calreticulin mutant stem cells recapitulate MPN hallmarks and identify targetable vulnerabilities.Semantic proximity Read ↗

Mutant Calreticulin in MPN: Mechanistic Insights and Therapeutic Implications.Semantic proximity Read ↗

Mutant calreticulin in myeloproliferative neoplasmsSemantic proximity Read ↗

Targeting the CALR interactome in myeloproliferative neoplasmsSemantic proximity Read ↗

Type I but Not Type II Calreticulin Mutations Activate the IRE1α/XBP1 Pathway of the Unfolded Protein Response to Drive Myeloproliferative Neoplasms.Semantic proximity Read ↗

Calreticulin Ins5 and Del52 mutations impair unfolded protein and oxidative stress responses in K562 cells expressing CALR mutantsSemantic proximity Read ↗

Mutant Calreticulin in the Myeloproliferative NeoplasmsSemantic proximity Read ↗

Selective targeting of mutated calreticulin by the monoclonal antibody INCA033989 inhibits oncogenic function of MPN.Semantic proximity Read ↗

The Role of Mutated Calreticulin in the Pathogenesis of BCR-ABL1-Negative Myeloproliferative Neoplasms.Semantic proximity Read ↗

Novel strategies targeting mutant calreticulin in essential thrombocythemia and myelofibrosis.Semantic proximity Read ↗

The role of calreticulin mutations in myeloproliferative neoplasms.Semantic proximity Read ↗

Calreticulin mutations in myeloproliferative neoplasms.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.