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accession-icon GSE1621
Differential expression of genes after 48 hrs, 10 d, and 3 wks of TAC
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Microarray analysis of gene expression after transverse aortic constriction in mice: comparison of TAC vs. sham group at 48 hours, 10 days, and 3 weeks.

Publication Title

Microarray analysis of gene expression after transverse aortic constriction in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP077724
ASXL1 Interacts with the Cohesin Complex to Maintain Chromatid Separation and Gene Expression for Normal Hematopoiesis [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

ASXL1 is frequently mutated in a spectrum of myeloid malignancies with poor prognosis. Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice, however, the underlying molecular mechanisms remain unclear. Here, we report that ASXL1 interacts with the cohesin complex, which has been shown to guide sister chromotid segregation and to regulate gene expression. Loss of Asxl1 impairs the cohesin function as reflected by an impaired telophase chromatid disjunction in hematopoietic cells. ChIP-seq data revealed that ASXL1, RAD21 and SMC1A share 93% of genomic binding sites at promoter regions in lineage-cKit+ (LK) cells. We have showed that loss of Asxl1 reduced the genome binding of RAD21 and SMC1A, and altered the expression of ASXL1/cohesin target genes in LK cells. Our study underscores the ASXL1-cohesin interaction as a novel means to maintain normal sister chromatid separation and to regulate gene expression in hematopoietic cells. Overall design: The DEG genes'' relation with the changes of ASXL1 peaks and Cohesin peaks changes

Publication Title

ASXL1 interacts with the cohesin complex to maintain chromatid separation and gene expression for normal hematopoiesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP125175
Tafazzin Regulates Cell State by Modulating Phosphatidylethanolamine and Phosphatidylserine levels
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Inhibiting tafazzin a cardiolipin remodeling enzyme reduces stemness of AML by modulating the level of phosphatidylserine Overall design: Gene expression analysis upon knock-down of TAZ by two independent shRNAs

Publication Title

The Mitochondrial Transacylase, Tafazzin, Regulates for AML Stemness by Modulating Intracellular Levels of Phospholipids.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE106800
Circadian misalignment induces fatty acid metabolism gene profiles and induces insulin resistance in human skeletal muscle.
  • organism-icon Homo sapiens
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Circadian misalignment, such as in shift work, has been associated with obesity and type 2 diabetes, however, direct effects of circadian misalignment on skeletal muscle insulin sensitivity and muscle molecular circadian clock have never been investigated in humans. Here we investigated insulin sensitivity and muscle metabolism in fourteen healthy young lean men (age 22.4 2.8 years; BMI 22.3 2.1 kg/m2 [mean SD]) after a 3-day control protocol and a 3.5-day misalignment protocol induced by a 12-h rapid shift of the behavioral cycle. We show that circadian misalignment results in a significant decrease in peripheral insulin sensitivity due to a reduced skeletal muscle non-oxidative glucose disposal (Rate of disappearance: 23.7 2.4 vs. 18.4 1.4 mg/kg/min; control vs. misalignment; p=0.024). Fasting glucose and FFA levels as well as sleeping metabolic rate were higher during circadian misalignment. Molecular analysis of skeletal muscle biopsies revealed that the molecular circadian clock was not aligned to the new behavourial rhythm, and microarray analysis revealed the human PPAR pathway as a key player in the disturbed energy metabolism upon circadian misallignement. Our findings may provide a mechanism underlying the increased risk of type 2 diabetes among shift workers.

Publication Title

Circadian misalignment induces fatty acid metabolism gene profiles and compromises insulin sensitivity in human skeletal muscle.

Sample Metadata Fields

Sex, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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