<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>25(18)</volume><submitter>Vadeikiene R</submitter><pubmed_abstract>Myeloproliferative neoplasms (MPNs) are characterized by increased proliferation of myeloid lineages in the bone marrow. Calreticulin (&lt;i>CALR&lt;/i>) 52 bp deletion and &lt;i>CALR&lt;/i> 5 bp insertion have been identified in essential thrombocythemia (ET) and primary myelofibrosis (PMF). There is not much data on the crosstalk between mutated &lt;i>CALR&lt;/i> and MPN-related signaling pathways, such as JAK/STAT, PI3K/Akt/mTOR, and Hedgehog. Calreticulin, a multifunctional protein, takes part in many cellular processes. Nevertheless, there is little data on how mutated &lt;i>CALR&lt;/i> affects the oxidative stress response and oxidative stress-induced DNA damage, apoptosis, and cell cycle progression. We aimed to investigate the role of the &lt;i>CALR&lt;/i> 52 bp deletion and 5 bp insertion in the pathogenesis o</pubmed_abstract><journal>International journal of molecular sciences</journal><pagination>9873</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11432199</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Role of Mutated Calreticulin in the Pathogenesis of &lt;i>BCR-ABL1&lt;/i>-Negative Myeloproliferative Neoplasms.</pubmed_title><pmcid>PMC11432199</pmcid><pubmed_authors>Laukaitiene D</pubmed_authors><pubmed_authors>Vadeikiene R</pubmed_authors><pubmed_authors>Satkauskas S</pubmed_authors><pubmed_authors>Ugenskiene R</pubmed_authors><pubmed_authors>Jakstys B</pubmed_authors><pubmed_authors>Juozaityte E</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Role of Mutated Calreticulin in the Pathogenesis of &lt;i>BCR-ABL1&lt;/i>-Negative Myeloproliferative Neoplasms.</name><description>Myeloproliferative neoplasms (MPNs) are characterized by increased proliferation of myeloid lineages in the bone marrow. Calreticulin (&lt;i>CALR&lt;/i>) 52 bp deletion and &lt;i>CALR&lt;/i> 5 bp insertion have been identified in essential thrombocythemia (ET) and primary myelofibrosis (PMF). There is not much data on the crosstalk between mutated &lt;i>CALR&lt;/i> and MPN-related signaling pathways, such as JAK/STAT, PI3K/Akt/mTOR, and Hedgehog. Calreticulin, a multifunctional protein, takes part in many cellular processes. Nevertheless, there is little data on how mutated &lt;i>CALR&lt;/i> affects the oxidative stress response and oxidative stress-induced DNA damage, apoptosis, and cell cycle progression. We aimed to investigate the role of the &lt;i>CALR&lt;/i> 52 bp deletion and 5 bp insertion in the pathogenesis o</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Sep</publication><modification>2026-05-14T03:15:49.825Z</modification><creation>2025-04-07T07:39:02.244Z</creation></dates><accession>S-EPMC11432199</accession><cross_references><pubmed>39337361</pubmed><doi>10.3390/ijms25189873</doi></cross_references></HashMap>