<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Olson AT</submitter><funding>NCI NIH HHS</funding><pubmed_abstract>Kaposi's sarcoma-associated herpesvirus (KSHV) causes several human diseases including Kaposi's sarcoma (KS), a leading cause of cancer in Africa and in patients with AIDS. KS tumor cells harbor KSHV predominantly in a latent form, while typically &lt;5% contain lytic replicating virus. Because both latent and lytic stages likely contribute to cancer initiation and progression, continued dissection of host regulators of this biological switch will provide insights into fundamental pathways controlling the KSHV life cycle and related disease pathogenesis. Several cellular protein kinases have been reported to promote or restrict KSHV reactivation, but our knowledge of these signaling mediators and pathways is incomplete. We employed a polypharmacology-based kinome screen to identifiy specific </pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2023.02.01.526589</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9915688</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Polypharmacology-based kinome screen identifies new regulators of KSHV reactivation.</pubmed_title><pmcid>PMC9915688</pmcid><funding_grant_id>R21 CA240479</funding_grant_id><funding_grant_id>R01 CA189986</funding_grant_id><funding_grant_id>P30 CA015704</funding_grant_id><funding_grant_id>R01 CA097934</funding_grant_id><funding_grant_id>R01 CA217788</funding_grant_id><pubmed_authors>Ladha AM</pubmed_authors><pubmed_authors>Lim CB</pubmed_authors><pubmed_authors>Olson AT</pubmed_authors><pubmed_authors>Gujral TS</pubmed_authors><pubmed_authors>Kang Y</pubmed_authors><pubmed_authors>Geballe AP</pubmed_authors><pubmed_authors>Lagunoff M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Polypharmacology-based kinome screen identifies new regulators of KSHV reactivation.</name><description>Kaposi's sarcoma-associated herpesvirus (KSHV) causes several human diseases including Kaposi's sarcoma (KS), a leading cause of cancer in Africa and in patients with AIDS. KS tumor cells harbor KSHV predominantly in a latent form, while typically &lt;5% contain lytic replicating virus. Because both latent and lytic stages likely contribute to cancer initiation and progression, continued dissection of host regulators of this biological switch will provide insights into fundamental pathways controlling the KSHV life cycle and related disease pathogenesis. Several cellular protein kinases have been reported to promote or restrict KSHV reactivation, but our knowledge of these signaling mediators and pathways is incomplete. We employed a polypharmacology-based kinome screen to identifiy specific </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2026-04-08T14:08:00.069Z</modification><creation>2025-02-19T04:20:59.504Z</creation></dates><accession>S-EPMC9915688</accession><cross_references><pubmed>36778430</pubmed><doi>10.1101/2023.02.01.526589</doi></cross_references></HashMap>