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Article

Lysosomal degradation targets mutant calreticulin and the thrombopoietin receptor in myeloproliferative neoplasms.

Blood advances - 9 Jul 2024

Kaur Amanpreet, Venkatesan Arunkumar, Kandarpa Malathi, Talpaz Moshe, Raghavan Malini

Abstract excerpt

ABSTRACT: Somatic mutants of calreticulin (CRT) drive myeloproliferative neoplasms (MPNs) via binding to the thrombopoietin receptor (MPL) and aberrant activation of the JAK/STAT pathway. Compared with healthy donors, platelets from mutant CRT-expressing patients with MPN display low cell surface MPL. Additionally, coexpression of MPL with an MPN-linked CRT mutant (CRTDel52) reduces cell surface MPL, suggesting...

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Share to Calreticulin
Share to Cell Proliferation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Mutation

Share to Myeloproliferative Disorders

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Share to Receptors, Thrombopoietin

Share to TOR Serine-Threonine Kinases

Source

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Identifiers

PMID: 38640435
DOI: 10.1182/bloodadvances.2023011432
PMCID: PMC11255115

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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