Ontology highlight
ABSTRACT:
PROVIDER: PRJNA245220 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of E18.5 livers derived from Wnt5a-deficient (KO) mice compared to those from littermate wild-type (WT) mice. RNA samples were extracted from whole livers derived from E18.5 fetuses. Two-condition experiment: Wnt5a KO vs. WT whole livers. Total RNA samples were extracted from E18.5 whole livers. KO and WT samples were a mixture of RNA solutions derived from two Wnt5a KO livers and two WT livers, respectively.
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Project description:We report ChIP-Seq data for C/EBPa in livers of mice with liver-specific KO (LSKO) of Trib1 as compared to WT controls, or in livers of mice overexpressing C/EBPa via adeno-associated virus (AAV) as compared to controls.
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Project description:Transcriptional profiling of E14 Dlk+ cells derived from Matrix metalloproteinase (MMP)-14 deficient (KO) mice comparing those from littermate wild-type (WT) mice. RNA samples were extrated from FACS-sorted Dlk+CD45-CD71-Ter119- cells derived from E14.5 livers. Transcriptional profiling of postnatal day (P)1 livers derived from MMP-14 deficient (KO) mice comparing those from littermate wild-type (WT) mice. RNA samples were extrated from whole livers derived from P1 mice.
2015-12-25 | GSE73943 | GEO
Project description:We report ChIP-Seq data for C/EBPa in livers of mice with liver-specific KO (LSKO) of Trib1 as compared to WT controls, or in livers of mice overexpressing C/EBPa via adeno-associated virus (AAV) as compared to controls. 8-10 week old Trib1 flox/flox mice treated with AAV_Null (WT) or AAV_Cre (LSKO); 8-10 week old C57B/6 WT mice treated with AAV_Null or AAV_Cebpa.
2015-07-14 | E-GEOD-70716 | biostudies-arrayexpress
Project description:To examine whether energy starvation caused by the increase in rRNA transcription affects liver metabolism, we compared the gene expression profiles of WT and NML-KO livers using Affymetrix microarray technology. We analyzed 5 livers of WT mice and 5 livers of NML-KO mice.
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Project description:Metabolic reprogramming in livers from LKB1 KO mice
| PRJNA791350 | ENA
Project description:MSI (Microsatellite Instability) colorectal cancer (CRC) show improved survival, are less prone to metastasis and show poor response to chemotherapy (compared to MSS tumors). The underlying reasons for these characteristics are still not understood and no specific therapeutic approach for MSI colon tumours (15% of CRC overall) has yet been developed.
The MSI process is oncogenic when it affects DNA repeat sequences that have a functional role, e.g. Small Coding Repeats (SCR). MSI also frequently affects Long Non-Coding Repeats (LNCR) in tumour DNA. In contrast to SCR, only a few LNCR are endowed with biological activity. Consequently, this area has received very little attention. Our group recently identified HSP110 mutant chaperone protein in MSI CRC that was generated by somatic deletion of a LNCR. Of interest, HSP110 mutant (due to exon skipping) have anti-oncogenic properties and the survival of MSI CRC patients receiving chemotherapy is positively associated with HSP110 mutations in tumour DNA.
The aim of the current project is to identify additional clinically relevant MSI-associated splicing aberrations due to mutations in LNCR located in splice acceptor sites. The four main steps are as follows:
1. To identify exon/intron sites affected by aberrant splicing events due to MSI in CRC . All RNASeq data will be exploited to identify recurrent splicing aberrations (mostly exon skipping) that occur specifically in MSI colon tumours;
2. To investigate for possible functional links between MSI and any detected aberrant splicing events . All specific aberrant splicing events detected by RNAseq in MSI CRC samples will be first confirmed (quantitative RT-PCR) in order to eliminate false positive cases. For validated exon candidates, the allelic profiles of adjacent intronic LNCR will be analysed (PCR and fluorescence genotyping) in CRC cell lines and primary tumours (MSI and MSS), as well as in matching normal mucosa samples in order to assess their polymorphic status;
3. To identify splicing events and LNCR mutations with clinical relevance in MSI CRC patients . All LNCR with a confirmed role in gene splicing in MSI CRC will be analysed. The clinical relevance of candidate genes will be assessed using multivariate survival regression models for Relapse- Free Survival, with interaction terms (response to chemotherapy);
4. To initiate functional studies on a limited number of clinically relevant, cancer-related genes whose splicing is perturbed in MSI cancer cells, and to develop biological tools to simplify screening in future clinical assays Similar to HSP110, we will focus on 4 or 5 mutant proteins that are promising drug therapeutic targets. Functional assays will be developed to further elucidate their role in the pathophysiology of MSI tumours. We also aim to develop biological tools for these candidate genes, such as the detection of wild-type or mutant proteins by immunohistochemistry.
| 2266966 | ecrin-mdr-crc
Project description:Transcriptional profiling of E18.5 livers derived from Wnt5a-deficient (KO) mice compared to those from littermate wild-type (WT) mice. RNA samples were extracted from whole livers derived from E18.5 fetuses.
2013-02-07 | GSE41803 | GEO
Project description:To identify aberrant splicing isoforms and potential neoantigens, we performed full-length cDNA sequencing of lung adenocarcinoma cell lines using a long-read sequencer MinION. We constructed a comprehensive catalog of aberrant splicing isoforms and detected isoform-specific peptides using proteome analysis.
2020-12-09 | PXD019915 | JPOST Repository