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Filename: drivers/Session_files_driver.php
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Filename: Session/Session.php
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Function: require_once
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Function: _error_handler
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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Filename: models/Detail_model.php
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Function: strpos
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Function: insertAPISummary
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Filename: helpers/my_audit_helper.php
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Function: str_replace
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Function: formatAIDetailSummary
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Filename: controllers/Detail.php
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File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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CREBBP (CBP/KAT3A) and its paralogue EP300 (KAT3B) are lysine acetyltransferases (KATs) that are essential for human development. They each comprise 10 domains through which they interact with >400 proteins, making them important transcriptional co-activators and key nodes in the human protein-protein interactome. The bromodomains of CREBBP and EP300 enable the binding of acetylated lysine residues from histones and a number of other important proteins, including p53, p73, E2F, and GATA1. Here, we report a work to develop a high-affinity, small-molecule ligand for the CREBBP and EP300 bromodomains [(-)-OXFBD05] that shows >100-fold selectivity over a representative member of the BET bromodomains, BRD4(1). Cellular studies using this ligand demonstrate that the inhibition of the CREBBP/EP300 bromodomain in HCT116 colon cancer cells results in lowered levels of c-Myc and a reduction in H3K18 and H3K27 acetylation. In hypoxia (<0.1% O), the inhibition of the CREBBP/EP300 bromodomain results in the enhanced stabilization of HIF-1α.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8311651 | PMC |
http://dx.doi.org/10.1021/acs.jmedchem.1c00348 | DOI Listing |
Integr Biol (Camb)
January 2024
Department of Biotechnology, School of Bioscience and Technology (SBST), Vellore Institute of Technology (VIT), Vellore District, Tamil Nadu State, 632014, India.
Acute myeloid leukemia (AML) accounts for 1.3% of all cancers, with a limited survival of only 30%, and treating AML is a continuous challenge in medicine. IKZF1 is a DNA-binding protein that is highly mutated and undruggable but significant in causing AML.
View Article and Find Full Text PDFWomen Health
December 2024
School Of Applied Sciences and Technology, Gujarat Technological University, Ahmedabad, India.
Biochem Biophys Res Commun
December 2024
Research Institute, National Cancer Center, Goyang-si, Gyeonggi-do, 10408, Republic of Korea; Department of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang-si, Gyeonggi-do, 10408, Republic of Korea. Electronic address:
Small-cell lung cancer (SCLC) is highly lethal because the tumors grow and metastasize rapidly. Effective treatments for SCLC are lacking currently. A recent study demonstrated that the E1A binding protein P300 (EP300) KIX domain has pro-tumorigenic activity and is selectively involved in the development and growth of SCLC.
View Article and Find Full Text PDFClin Genet
November 2024
Department of Neurosciences Rita Levi-Montalcini, University of Turin, Turin, Italy.
Rubinstein-Taybi syndrome (RSTS) is a rare autosomal dominant neurodevelopmental disorder linked to haploinsufficiency of CREBBP (RSTS1) and EP300 (RSTS2) genes. Characteristic features often include distinctive facial traits, broad thumbs and toes, short stature, and various degrees of intellectual disability. The clinical presentation of RSTS is notably variable, making it challenging to establish a clear genotype-phenotype correlation, except for specific variants which cause the allelic Menke-Hennekam syndrome.
View Article and Find Full Text PDFLeuk Lymphoma
November 2024
Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
ZNF384 gene rearrangements are a distinct subtype of adult B cell acute lymphoblastic leukemia (B-ALL). We screened 46 B-other ALL patients for fusions using fluorescent hybridization (FISH) and reverse transcription-polymerase chain reaction (RT-PCR). Clinical data, treatment response, and minimal residual disease (MRD) status were analyzed.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!