{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["14"],"submitter":["Fu W"],"pubmed_abstract":["<h4>Background</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.<h4>Methods</h4>Using RT-PCR, we amplified full-length human FHL1C, and con"],"journal":["BMC cancer"],"pagination":["463"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4077834"],"repository":["biostudies-literature"],"pubmed_title":["FHL1C induces apoptosis in Notch1-dependent T-ALL cells through an interaction with RBP-J."],"pmcid":["PMC4077834"],"pubmed_authors":["Zhao JL","Yu HC","Li SZ","Fu W","Huang SY","Liang L","Han H","Qin HY","Lin Y","Liang YM","Wang K"],"additional_accession":[]},"is_claimable":false,"name":"FHL1C induces apoptosis in Notch1-dependent T-ALL cells through an interaction with RBP-J.","description":"<h4>Background</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.<h4>Methods</h4>Using RT-PCR, we amplified full-length human FHL1C, and con","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jun","modification":"2026-05-03T23:27:09.112Z","creation":"2019-03-27T01:31:14Z"},"accession":"S-EPMC4077834","cross_references":{"pubmed":["24952875"],"doi":["10.1186/1471-2407-14-463"]}}