Effects of fasting on gene expression from livers with or without Mcl1 genetic deletion
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ABSTRACT:
PROVIDER: PRJNA933619 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MCL-1 is an essential pro-survival molecule of the BCL-2 family of proteins. Recent data, however, suggest it may play an as-yet unclarified role in mitochondrial metabolism. Liver-specific deletion of MCL-1 followed by dietary stress leads to alteration of multiple genetic programs including fatty acid metabolic processes.
2024-03-19 | GSE225055 | GEO
Project description:We report the RNA sequencing results of four fasting mice with humanized livers and four fed mice with humanized livers.
2019-10-04 | GSE126587 | GEO
Project description:Fasting Fed RNA sequencing experiment of mice with humanized livers
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Project description:Fasting/fed/refeeding RNAseq experiment conducted on mice with xenografted human livers.
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Project description:The effect of resection of mouse livers on survival serve as a model for the effect of resection of human livers, which are performed for both the purposes of removing sick tissue and for transplanting healthy tissue. When less than 70% of a mouse liver is resected, the mouse usually lives. However, when more than 70% is resected, there is an increased probability that the mouse will die. We have found that deletion of Ager (Advanced Glycation End products receptor) (Rage) increases the chance of mouse survival relavtive to WT. Conversely, the deletion of Myd88 decreases the chances of survival, as does the simultaneous deletion of both Ager and Myd88. To understand these genotype/phenotype relations, we performed gene expression measurements.
2012-06-26 | GSE22873 | GEO
Project description:The anti-apoptotic MCL1 protein is a member of the pro-survival BCL2 family and is frequently amplified or elevated in human cancers. MCL1 protein is highly unstable, with its stability being regulated by phosphorylation and ubiquitination. We attempted to identify acetylation as another critical post-translational modification regulating MCL1 protein stability. To this end, 293T cells were transfected with HA-humanMCL1 and Myc-p300. The whole-cell lysates were immunoprecipitated with anti-HA agarose beads. The immunoprecipitated material was resolved by SDS-PAGE, and the MCL1 band was excised for tryptic digestion followed by the MS analysis.
2021-10-14 | MSV000088231 | MassIVE
Project description:MCL1 is an anti-apoptotic member of the BCL2 family that is deregulated in various solid and hematological malignancies. However, its role in the molecular pathogenesis of diffuse large B-cell lymphoma (DLBCL) is unclear. We analyzed gene expression profiling data from 350 DLBCL patient samples and detected that activated B-cell-like (ABC) DLBCLs express MCL1 at significantly higher levels compared to germinal center B-cell-like (GCB) DLBCL patient samples (p=2.7 x 10(-10)) [PMID 23257783]. Immunohistochemistry confirmed high MCL1 protein expression predominantly in ABC DLBCL in an independent patient cohort (n=249; p=0.001). To elucidate molecular mechanisms leading to aberrant MCL1 expression, we analyzed array comparative genomic hybridization (aCGH) data of 203 DLBCL samples [GSE11318] and identified recurrent chromosomal gains/amplifications of the MCL1 locus that occurred in 26% of ABC DLBCLs. In addition, aberrant STAT3 signaling contributed to high MCL1 expression in this subtype. Knockdown of MCL1 as well as treatment with the BH3-mimetic obatoclax induced apoptotic cell death in MCL1 positive DLBCL cell lines. In summary, MCL1 is deregulated in a significant fraction of ABC DLBCLs and contributes to therapy resistance. These data suggest that specific inhibition of MCL1 might be utilized therapeutically in a subset of DLBCLs. This GEO dataset is comprised of aCGH measurements for DLBCL cell lines, which are used in the above-mentioned paper. Cell lines were measured against the DNA of a healthy male donor who in turn was measured against a pool of healthy DNAs to correct for individual CNVs of the donor.
2013-01-04 | E-GEOD-43272 | biostudies-arrayexpress
Project description:The effect of resection of mouse livers on survival serve as a model for the effect of resection of human livers, which are performed for both the purposes of removing sick tissue and for transplanting healthy tissue. When less than 70% of a mouse liver is resected, the mouse usually lives. However, when more than 70% is resected, there is an increased probability that the mouse will die. We have found that deletion of Ager (Advanced Glycation End products receptor) (Rage) increases the chance of mouse survival relavtive to WT. Conversely, the deletion of Myd88 decreases the chances of survival, as does the simultaneous deletion of both Ager and Myd88. To understand these genotype/phenotype relations, we performed gene expression measurements. Gene expression of livers of WT C57BL/6 mice, Ager-null C57BL/6 mice, Myd88-null C57BL/6 mice, and Ager-null/Myd88-null C57BL/6 mice, all 10-12 weeks-old and sacrificed 2 hours after 85% liver resection, were compared. 4-6 replicates each group.
2012-06-25 | E-GEOD-22873 | biostudies-arrayexpress
Project description:MCL1 is an anti-apoptotic member of the BCL2 family that is deregulated in various solid and hematological malignancies. However, its role in the molecular pathogenesis of diffuse large B-cell lymphoma (DLBCL) is unclear. We analyzed gene expression profiling data from 350 DLBCL patient samples and detected that activated B-cell-like (ABC) DLBCLs express MCL1 at significantly higher levels compared to germinal center B-cell-like (GCB) DLBCL patient samples (p=2.7 x 10(-10)) [PMID 23257783]. Immunohistochemistry confirmed high MCL1 protein expression predominantly in ABC DLBCL in an independent patient cohort (n=249; p=0.001). To elucidate molecular mechanisms leading to aberrant MCL1 expression, we analyzed array comparative genomic hybridization (aCGH) data of 203 DLBCL samples [GSE11318] and identified recurrent chromosomal gains/amplifications of the MCL1 locus that occurred in 26% of ABC DLBCLs. In addition, aberrant STAT3 signaling contributed to high MCL1 expression in this subtype. Knockdown of MCL1 as well as treatment with the BH3-mimetic obatoclax induced apoptotic cell death in MCL1 positive DLBCL cell lines. In summary, MCL1 is deregulated in a significant fraction of ABC DLBCLs and contributes to therapy resistance. These data suggest that specific inhibition of MCL1 might be utilized therapeutically in a subset of DLBCLs.
2013-01-04 | GSE43272 | GEO
Project description:To get insight into the mechanisms of MCL1-induced survival and transformation, we screened 41,000 human genes in a genome-wide gene expression profile analysis of MCL1 over-expressing B-NHL cells. Experiment Overall Design: Two-color (Cy5-CTP/ Cy3-CTP) microarray-based gene expression formats presenting high-density oligonucleotide probes printed on a single glass slide were used (Agilent technologies, Cat No# G4112A whole human genome 41K). Total RNAs from MCL1 over-expressing RAMOS RA-1 and Z-138 B-cells were labeled with Cy5-CTP, whereas RNAs from references (empty vector/ RAMOS RA-1 and empty vector/ Z-138 B-cells) were labeled with Cy3-CTP. After competitive hybridization [RNA-Cy5 from MCL1 over-expressing RAMOS RA-1 or MCL1 over-expressing Z-138 versus RNA-Cy3 from either empty vector/ RAMOS RA-1 or empty vector/ Z-138 respectively] gene expression data were pre-processed using Feature Extraction software and GEPAS tools (http://gepas.bioinfo.cipf.es/).
2008-06-16 | E-GEOD-8834 | biostudies-arrayexpress