<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>43(4)</volume><submitter>Zhu J</submitter><pubmed_abstract>Newborns suffering from hypoxia-ischemia (HI) brain injury still lack effective treatment. Proline-rich tyrosine kinase 2 (Pyk2) is a non-receptor tyrosine kinase, which is highly correlated with transient ischemic brain injury in adult. In this study, we investigated the role of Pyk2 in neonatal HI brain injury. HI was induced in postnatal day 7 mouse pups by unilateral common carotid artery ligation followed by hypoxic exposure. Pyk2 interference lentivirus (LV-Pyk2 shRNA) was constructed and injected into unilateral cerebral ventricle of neonatal mice before HI. Infarct volume, pathological changes, and neurological behaviors were assessed on postnatal day 8-14. We showed that the phosphorylation level of Pyk2 was significantly increased in neonatal brain after HI, whereas LV-Pyk2 shRNA</pubmed_abstract><journal>Acta pharmacologica Sinica</journal><pagination>797-810</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8976000</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Pyk2 inhibition attenuates hypoxic-ischemic brain injury in neonatal mice.</pubmed_title><pmcid>PMC8976000</pmcid><pubmed_authors>Chu SF</pubmed_authors><pubmed_authors>Peng Y</pubmed_authors><pubmed_authors>Zhu J</pubmed_authors><pubmed_authors>Liu DD</pubmed_authors><pubmed_authors>Feng ZP</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Jian WX</pubmed_authors><pubmed_authors>Chen NH</pubmed_authors><pubmed_authors>Sun HS</pubmed_authors><pubmed_authors>Chen C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Pyk2 inhibition attenuates hypoxic-ischemic brain injury in neonatal mice.</name><description>Newborns suffering from hypoxia-ischemia (HI) brain injury still lack effective treatment. Proline-rich tyrosine kinase 2 (Pyk2) is a non-receptor tyrosine kinase, which is highly correlated with transient ischemic brain injury in adult. In this study, we investigated the role of Pyk2 in neonatal HI brain injury. HI was induced in postnatal day 7 mouse pups by unilateral common carotid artery ligation followed by hypoxic exposure. Pyk2 interference lentivirus (LV-Pyk2 shRNA) was constructed and injected into unilateral cerebral ventricle of neonatal mice before HI. Infarct volume, pathological changes, and neurological behaviors were assessed on postnatal day 8-14. We showed that the phosphorylation level of Pyk2 was significantly increased in neonatal brain after HI, whereas LV-Pyk2 shRNA</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2026-03-16T09:35:17.8Z</modification><creation>2025-04-06T00:04:54.69Z</creation></dates><accession>S-EPMC8976000</accession><cross_references><pubmed>34226665</pubmed><doi>10.1038/s41401-021-00694-5</doi></cross_references></HashMap>