<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pierre-Louis E</submitter><funding>NIAID NIH HHS</funding><funding>HHS | NIH | National Institute of Allergy and Infectious Diseases</funding><pagination>e0016022</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9241542</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7(3)</volume><pubmed_abstract>The protozoan Toxoplasma gondii is a highly successful obligate intracellular parasite that, upon invasion of its host cell, releases an array of host-modulating protein effectors to counter host defenses and further its own replication and dissemination. Early studies investigating the impact of T. gondii infection on host cell function revealed that this parasite can force normally quiescent cells to activate their cell cycle program. Prior reports by two independent groups identified the dense granule protein effector HCE1/TEEGR as being solely responsible for driving host cell transcriptional changes through its direct interaction with the cyclin E regulatory complex DP1 and associated transcription factors. Our group independently identified HCE1/TEEGR through the presence of distinct</pubmed_abstract><journal>mSphere</journal><pubmed_title>Disruption of Toxoplasma gondii-Induced Host Cell DNA Replication Is Dependent on Contact Inhibition and Host Cell Type.</pubmed_title><pmcid>PMC9241542</pmcid><funding_grant_id>R21 AI142431</funding_grant_id><funding_grant_id>T32 AI060546</funding_grant_id><funding_grant_id>R21AI142431</funding_grant_id><funding_grant_id>T32AI060546</funding_grant_id><pubmed_authors>Etheridge MG</pubmed_authors><pubmed_authors>Chasen NM</pubmed_authors><pubmed_authors>Pierre-Louis E</pubmed_authors><pubmed_authors>de Paula Baptista R</pubmed_authors><pubmed_authors>Etheridge RD</pubmed_authors><pubmed_authors>Khan A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Disruption of Toxoplasma gondii-Induced Host Cell DNA Replication Is Dependent on Contact Inhibition and Host Cell Type.</name><description>The protozoan Toxoplasma gondii is a highly successful obligate intracellular parasite that, upon invasion of its host cell, releases an array of host-modulating protein effectors to counter host defenses and further its own replication and dissemination. Early studies investigating the impact of T. gondii infection on host cell function revealed that this parasite can force normally quiescent cells to activate their cell cycle program. Prior reports by two independent groups identified the dense granule protein effector HCE1/TEEGR as being solely responsible for driving host cell transcriptional changes through its direct interaction with the cyclin E regulatory complex DP1 and associated transcription factors. Our group independently identified HCE1/TEEGR through the presence of distinct</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2026-06-15T05:57:00.058Z</modification><creation>2024-11-13T21:48:10.816Z</creation></dates><accession>S-EPMC9241542</accession><cross_references><pubmed>35587658</pubmed><doi>10.1128/msphere.00160-22</doi></cross_references></HashMap>