Duke CC
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1055131 | ENA |
REPOSITORIES: ENA
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Project description:Duke Vaccine Manufacturing and Toxicology Core (Duke VMTC)
| PRJNA1055133 | ENA
Project description:University of Maryland School of Medicine, CIVICs Clinical Core (UMB CC)
| PRJNA1055132 | ENA
Project description:These samples are being analyzed by the Duke-UNC-Texas-EBI ENCODE consortium. Expression from these cell types will compared to three whole genome open chromatin methodologies: DNaseI hypersensitivity (DNase-seq), Formaldehyde-Assisted Isolation of Regulatory elements (FAIRE-seq), and Chromatin Immunoprecipitation (ChIP-seq) . For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
2009-04-23 | GSE15805 | GEO
Project description:To investigate the CMS subtype of the CC-531 cells, CC-531 organoids and CC-531 ex vivo tumor tissue grown in the peritoneum of WAG/Rij rats We then performed gene expression profiling analysis using data obtained from RNA-seq of CC-531 cells, CC-531 organoids and CC-531 ex vivo tumor tissue grown in the peritoneum of WAG/Rij rats of three different passages per sample type.
2023-03-03 | GSE226558 | GEO
Project description:CC-122 is a next-generation cereblon E3 ligase modulating agent that has demonstrated promising clinical efficacy in relapsed or refractory diffuse large B‐cell lymphoma (R/R DLBCL) patients. Mechanistically, CC-122 induces the degradation of IKZF1/3, leading to T cell activation and robust cell-autonomous killing in DLBCL. Here, we report a genome-wide CRISPR/Cas9 positive selection screen for CC-122 in a DLBCL cell line SU-DHL-4 with follow-up mechanistic characterization in 6 DLBCL cell lines to identify genes regulating the response to CC-122. Top-ranked CC-122 resistance genes encode not only well-defined members or regulators of the CUL4-DDB1-RBX1-CRBN E3 ubiquitin ligase complex, but also key components of several signaling and transcriptional networks that have not previously been shown to modulate the response to other cereblon modulators. Ablation of CYLD, NFKBIA, TRAF2, or TRAF3 induces hyper-activation of the canonical and/or non-canonical NF-κB pathways and subsequently diminishes CC-122-induced apoptosis in 5 out of 6 DLBCL cell lines. Depletion of KCTD5, the substrate receptor of the CUL3-RBX1-KCTD5 ubiquitin ligase complex, promotes the stabilization of its cognate substrate, GNG5, resulting in CC-122 resistance in HT, SU-DHL-4, and WSU-DLCL2. Furthermore, knockout of AMBRA1 renders resistance to CC-122 in SU-DHL-4 and U-2932, whereas knockout of RFX7 leads to resistance specifically in SU-DHL-4. The ubiquitous and cell line-specific mechanisms of CC-122 resistance in DLBCL cell lines revealed in this work pinpoint genetic alternations that are potentially associated with clinical resistance in patients, and facilitate the development of biomarker strategies for patient stratification, which may improve clinical outcome of CC-122 for R/R DLBCL.
2020-10-01 | GSE158303 | GEO
Project description:Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality, necessitating innovative therapeutic approaches. This study demonstrates that the compound CC-885 exerts potent anti-tumor effects in HCC both in vitro and in vivo. CC-885 significantly inhibited proliferation, migration, and invasion of HCC cells. In vivo, CC-885 markedly reduced tumor growth and angiogenesis in chick embryo and mouse xenograft models. Mechanistically, CC-885 selectively reduced GOLM1 protein levels via ubiquitin-mediated proteasomal degradation, without affecting its mRNA levels. GOLM1 knockdown mimicked the anti-proliferative effects of CC-885, while overexpression of GOLM1 conferred resistance to CC-885-induced apoptosis and growth inhibition. CC-885 facilitated the interaction between GOLM1 and the E3 ubiquitin ligase CRBN, promoting GOLM1 ubiquitination and degradation. Transcriptomic analyses revealed that CC-885 and GOLM1 knockdown modulated key pathways involved in apoptosis, NF-κB signaling, and cell proliferation. These findings highlight CC-885 as a promising therapeutic agent for HCC, primarily by facilitating the CRBN-dependent degradation of GOLM1, underscoring its potential for clinical application.
2024-10-11 | GSE272556 | GEO
Project description:Chlamydomonas reinhardtii CC-425 x CC-124 transcriptome
| PRJNA370690 | ENA
Project description:Antimicrobial peptides (AMPs) are compounds with a variety of bioactive properties. Especially promising are their antibacterial activities, often towards drug-resistant pathogens. Across different AMP sources, AMPs expressed within plants are relatively underexplored, with a limited number of plant AMP families identified. Recently, we identified the novel AMPs CC-AMP1 and CC-AMP2 in ghost pepper plants (Capsicum chinense x frutescens), exerting promising antibacterial activity and not classifying into any known plant AMP family. Herein, AMPs related to CC-AMP1 and CC-AMP2 were identified within both Capsicum annuum and Capsicum baccatum. Targeted MS/MS experiments were performed to determine peptide sequences, guided by in silico AMP sequence predictions.
2024-01-27 | PXD041035 | Pride
Project description:Platelet-derived growth factor-CC (PDGF-CC) is the third member of the PDGF family discovered after more than two decades of studies on the original members of the family, PDGF-AA and PDGF-BB. The biological function of PDGF-CC remains largely to be explored. We report here a novel finding that PDGF-CC is a potent neuroprotective factor that acts by modulating glycogen synthase kinase (GSK)3beta activity. In several different animal models of neuronal injury, such as axotomy-induced neuronal death, neurotoxin-induced neuronal injury, 6-OHDA-induced Parkinson's dopaminergic neuronal death and ischemia-induced stroke, PDGF-CC protein or gene delivery protected different types of neurons from apoptosis in both the retina and brain. On the other hand, loss-of-function assays using PDGF-C null mice, neutralizing antibody or shRNA showed that PDGF-CC deficiency/inhibition exacerbated neuronal death in different neuronal tissues in vivo. Mechanistically, we revealed that the neuroprotective effect of PDGF-CC was achieved by regulating GSK3beta phosphorylation and expression. Our data demonstrate that PDGF-CC is critically required for neuronal survival, and may potentially be used to treat neurodegenerative diseases. Inhibition of the PDGF-CC/receptor pathway for different clinical purposes should be conducted with caution to preserve normal neuronal functions.
2010-02-26 | GSE19207 | GEO