<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14</volume><submitter>Fu W</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Aberrantly activated Notch signaling has been found in more than 50% of patients with T-cell acute lymphoblastic leukemia (T-ALL). Current strategies that employ γ-secretase inhibitors (GSIs) to target Notch activation have not been successful. Many limitations, such as non-Notch specificity, dose-limiting gastrointestinal toxicity and GSI resistance, have prompted an urgent need for more effective Notch signaling inhibitors for T-ALL treatment. Human four-and-a-half LIM domain protein 1C (FHL1C) (KyoT2 in mice) has been demonstrated to suppress Notch activation in vitro, suggesting that FHL1C may be new candidate target in T-ALL therapy. However, the role of FHL1C in T-ALL cells remained unclear.&lt;h4>Methods&lt;/h4>Using RT-PCR, we amplified full-length human FHL1C, and con</pubmed_abstract><journal>BMC cancer</journal><pagination>463</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4077834</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>FHL1C induces apoptosis in Notch1-dependent T-ALL cells through an interaction with RBP-J.</pubmed_title><pmcid>PMC4077834</pmcid><pubmed_authors>Zhao JL</pubmed_authors><pubmed_authors>Yu HC</pubmed_authors><pubmed_authors>Li SZ</pubmed_authors><pubmed_authors>Fu W</pubmed_authors><pubmed_authors>Huang SY</pubmed_authors><pubmed_authors>Liang L</pubmed_authors><pubmed_authors>Han H</pubmed_authors><pubmed_authors>Qin HY</pubmed_authors><pubmed_authors>Lin Y</pubmed_authors><pubmed_authors>Liang YM</pubmed_authors><pubmed_authors>Wang K</pubmed_authors></additional><is_claimable>false</is_claimable><name>FHL1C induces apoptosis in Notch1-dependent T-ALL cells through an interaction with RBP-J.</name><description>&lt;h4>Background&lt;/h4>Aberrantly activated Notch signaling has been found in more than 50% of patients with T-cell acute lymphoblastic leukemia (T-ALL). Current strategies that employ γ-secretase inhibitors (GSIs) to target Notch activation have not been successful. Many limitations, such as non-Notch specificity, dose-limiting gastrointestinal toxicity and GSI resistance, have prompted an urgent need for more effective Notch signaling inhibitors for T-ALL treatment. Human four-and-a-half LIM domain protein 1C (FHL1C) (KyoT2 in mice) has been demonstrated to suppress Notch activation in vitro, suggesting that FHL1C may be new candidate target in T-ALL therapy. However, the role of FHL1C in T-ALL cells remained unclear.&lt;h4>Methods&lt;/h4>Using RT-PCR, we amplified full-length human FHL1C, and con</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jun</publication><modification>2026-05-03T23:27:09.112Z</modification><creation>2019-03-27T01:31:14Z</creation></dates><accession>S-EPMC4077834</accession><cross_references><pubmed>24952875</pubmed><doi>10.1186/1471-2407-14-463</doi></cross_references></HashMap>