<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16</volume><submitter>Xu X</submitter><pubmed_abstract>The relationship between calcium oscillation and cell sensitivity is poorly understood. Calcium oscillation can occur spontaneously or be triggered upon receptor-ligand binding. The cytosolic [Ca&lt;sup>2+&lt;/sup>] increase during calcium oscillation is initiated from Ca&lt;sup>2+&lt;/sup> release from the intracellular stores through the phospholipase C (PLC)-derived inositol 1,4,5-trisphosphate (IP&lt;sub>3&lt;/sub>). Here, we show that neutrophil-like HL60 cells lacking PLCγ2 (&lt;i>plcg2&lt;sup>kd&lt;/sup>&lt;/i> ) exhibit impaired spontaneous calcium oscillation and a diminished calcium response to chemoattractant stimulation. These defects result in reduced membrane targeting of RasGAP CAPRI (calcium-promoted Ras inactivator), and subsequent elevated Ras activations and enhanced downstream signaling, including P</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1633390</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12354650</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>PLCγ2 controls neutrophil-like cell sensitivity through calcium oscillation and gates chemoattractant concentration range for chemotaxis.</pubmed_title><pmcid>PMC12354650</pmcid><pubmed_authors>Lee A</pubmed_authors><pubmed_authors>Jin T</pubmed_authors><pubmed_authors>Kim WS</pubmed_authors><pubmed_authors>Xu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>PLCγ2 controls neutrophil-like cell sensitivity through calcium oscillation and gates chemoattractant concentration range for chemotaxis.</name><description>The relationship between calcium oscillation and cell sensitivity is poorly understood. Calcium oscillation can occur spontaneously or be triggered upon receptor-ligand binding. The cytosolic [Ca&lt;sup>2+&lt;/sup>] increase during calcium oscillation is initiated from Ca&lt;sup>2+&lt;/sup> release from the intracellular stores through the phospholipase C (PLC)-derived inositol 1,4,5-trisphosphate (IP&lt;sub>3&lt;/sub>). Here, we show that neutrophil-like HL60 cells lacking PLCγ2 (&lt;i>plcg2&lt;sup>kd&lt;/sup>&lt;/i> ) exhibit impaired spontaneous calcium oscillation and a diminished calcium response to chemoattractant stimulation. These defects result in reduced membrane targeting of RasGAP CAPRI (calcium-promoted Ras inactivator), and subsequent elevated Ras activations and enhanced downstream signaling, including P</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-05-02T02:47:18.573Z</modification><creation>2026-04-07T17:34:41.812Z</creation></dates><accession>S-EPMC12354650</accession><cross_references><pubmed>40821808</pubmed><doi>10.3389/fimmu.2025.1633390</doi></cross_references></HashMap>