<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kang X</submitter><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>Leukemia and Lymphoma Society</funding><pagination>30</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5828341</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>We recently identified the human leukocyte immunoglobulin-like receptor B2 (LILRB2) and its mouse ortholog-paired Ig-like receptor (PirB) as receptors for several angiopoietin-like proteins (Angptls). We also demonstrated that PirB is important for the development of acute myeloid leukemia (AML), but exactly how an inhibitory receptor such as PirB can support cancer development is intriguing.&lt;h4>Results&lt;/h4>Here, we showed that the activation of Ca (2+)/calmodulin-dependent protein kinases (CAMKs) is coupled with PirB signaling in AML cells. High expression of CAMKs is associated with a poor overall survival probability in patients with AML. Knockdown of CAMKI or CAMKIV decreased human acute leukemia development in vitro and in vivo. Mouse AML cells that are defective in</pubmed_abstract><journal>Journal of hematology &amp; oncology</journal><pubmed_title>CAMKs support development of acute myeloid leukemia.</pubmed_title><pmcid>PMC5828341</pmcid><funding_grant_id>R01 CA172268</funding_grant_id><funding_grant_id>1R01CA172268</funding_grant_id><funding_grant_id>1024-14</funding_grant_id><pubmed_authors>Zhang CC</pubmed_authors><pubmed_authors>Kang X</pubmed_authors><pubmed_authors>Muschen M</pubmed_authors><pubmed_authors>Huang J</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Lu Z</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Wu G</pubmed_authors><pubmed_authors>Wang L</pubmed_authors><pubmed_authors>Wang HY</pubmed_authors><pubmed_authors>Zhao M</pubmed_authors><pubmed_authors>Geng H</pubmed_authors><pubmed_authors>Chen Z</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Cui C</pubmed_authors></additional><is_claimable>false</is_claimable><name>CAMKs support development of acute myeloid leukemia.</name><description>&lt;h4>Background&lt;/h4>We recently identified the human leukocyte immunoglobulin-like receptor B2 (LILRB2) and its mouse ortholog-paired Ig-like receptor (PirB) as receptors for several angiopoietin-like proteins (Angptls). We also demonstrated that PirB is important for the development of acute myeloid leukemia (AML), but exactly how an inhibitory receptor such as PirB can support cancer development is intriguing.&lt;h4>Results&lt;/h4>Here, we showed that the activation of Ca (2+)/calmodulin-dependent protein kinases (CAMKs) is coupled with PirB signaling in AML cells. High expression of CAMKs is associated with a poor overall survival probability in patients with AML. Knockdown of CAMKI or CAMKIV decreased human acute leukemia development in vitro and in vivo. Mouse AML cells that are defective in</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Feb</publication><modification>2025-04-21T20:09:24.019Z</modification><creation>2019-03-26T23:04:27Z</creation></dates><accession>S-EPMC5828341</accession><cross_references><pubmed>29482582</pubmed><doi>10.1186/s13045-018-0574-8</doi></cross_references></HashMap>