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accession-icon GSE59545
NF-kB in Tumor Initiation
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

p65-/-Ras cells show delayed tumor formation in SCID mice. However, after prolonged latency, tumor formation was observed from these mice. To understand the changes of NF-kB regulated genes before and after tumor formation, RNA from p65+/+Ras, p65+/+RasTumor, p65-/-Ras, p65-/-RasTumor cells were isolated and microarray were performed.

Publication Title

NF-κB functions in tumor initiation by suppressing the surveillance of both innate and adaptive immune cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE30363
IKKa-mediated signaling circuitry regulates early B lymphopoiesis during hematopoiesis
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Multiple transcription factors regulate B cell commitment, which coordinates with myeloiderythroid lineage differentiation. One such factor, NF-kB, has long been speculated to regulate early B cell development; however, this issue remains controversial. IKKa is required for splenic B cell maturation, but not for bone marrow (BM) B cell development. Here, we unexpectedly found defective BM B cell development and an increased myeloiderythroid lineages in kinase-dead IKKa (KA/KA) knock-in mice. Markedly increased cytosolic p100, an NF-kB2 inhibitory form, and reduced nuclear NF-kB p65, RelB, p50, and p52, as well as IKKa, was observed in KA/KA splenic and BM B cells. Several B- and myeloiderythroid-cell regulators, including Pax5, were deregulated in KA/KA BM B cells. Using fetal liver and BM congenic transplants, and IKKa deletion from early hematopoietic cells in mice, this defect was identified as B cell intrinsic and as an early event during hematopoiesis. Re-expression of IKKa, Pax5, or combined NF-kB molecules promoted B cell development, but repressed myeloiderythroid cell differentiation in KA/KA BM B cells. Together, these results demonstrate that IKKa regulates B-lineage commitment via combined canonical and noncanonical NF-kB transcriptional activity to target Pax5 expression during hematopoiesis.

Publication Title

IKKα-mediated signaling circuitry regulates early B lymphopoiesis during hematopoiesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE70822
Expression data from human primary skeletal muscle myotubes treated with aldosterone, spironolactone, or vehicle.
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

To test for a function effect of mineralocorticoid receptor modulation in skeletal muscle, global gene expression analysis was conducted on human myltubes treated with a mineralocorticoid receptor agonist or antagonist.

Publication Title

Mineralocorticoid receptors are present in skeletal muscle and represent a potential therapeutic target.

Sample Metadata Fields

Sex

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accession-icon GSE70984
Expression data from quadriceps of utrn+/-;mdx mice treated with spironolactone plus lisinopril compared to untreated
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To identify the gene expression differences in skeletal muscles resulting from treatment of dystrophic mice with spironolactone plus lisinopril

Publication Title

Mineralocorticoid receptors are present in skeletal muscle and represent a potential therapeutic target.

Sample Metadata Fields

Sex, Age, Treatment

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accession-icon GSE75774
Expression data from mouse neonatal hindlimb muscles
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

During neonatal development, skeletal muscle grows dramatically by myonuclei accretion to existing fibers and hypertophic growth of fibers with protein synthesis.

Publication Title

An NF-κB--EphrinA5-Dependent Communication between NG2(+) Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates.

Sample Metadata Fields

Specimen part

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accession-icon SRP067169
RNAseq from neonatal mouse hindlimb muscles
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

During neonatal development, skeletal muscle grows dramatically by myonuclei accretion to existing fibers and hypertophic growth of fibers with protein synthesis. Overall design: To understand molecular mechanism underlying neonatal muscle growth, we used RNAseq to profile the global program of gene expressions especially involved in myoblast fusion, migration, and muscle fiber growth by itself. We used two biological replicates for each time point.

Publication Title

An NF-κB--EphrinA5-Dependent Communication between NG2(+) Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE18832
mRNA profiling in rectus abdominis muscle from patients with upper GI cancer
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Rectus abdominis muscle biopsies were obtained from 65 upper gastrointestinal (UGI) cancer patients during open surgery and RNA profiling was performed on a subset of this cohort (n=21) using the Affymetrix U133+2 platform with the aim of identifying biomarkers of cancer related muscle wasting.

Publication Title

Using transcriptomics to identify and validate novel biomarkers of human skeletal muscle cancer cachexia.

Sample Metadata Fields

Sex, Age, Specimen part, Disease

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accession-icon SRP111473
RNA Sequencing looking at differential gene expression between p65+/+ and p65-/- mouse embryonic fibroblasts (MEFs)
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We look at differential gene expression between immortalized p65+/+ and p65-/- MEFs to identify potential NF-kB regulated genes which when grouped based on biological function indicates candidates involved in protecting p65+/+ cells from macrophage-mediated killing Overall design: Examination of differential gene expression between two cell types either in the presence or absence of p65

Publication Title

NF-κB regulates GDF-15 to suppress macrophage surveillance during early tumor development.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE114026
7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKK
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

NF-κB inhibition rescues cardiac function by remodeling calcium genes in a Duchenne muscular dystrophy model.

Sample Metadata Fields

Age

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accession-icon GSE114025
Expression data from 7-month-old mdx mouse hearts wild-type and deficient for cardiomyocyte-specific IKK
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found genetic deletion of IKK in mdx cardiomyocytes improved cardiac function and normalized calcium transients. We used microarrays to profile gene expression in hearts of mdx mice with intact IKK signaling and hearts of mdx mice with IKK-deficient cardiomyocytes to identify genes differentially regulated by NF-[kappa]B. signaling in dystrophic hearts.

Publication Title

NF-κB inhibition rescues cardiac function by remodeling calcium genes in a Duchenne muscular dystrophy model.

Sample Metadata Fields

Age

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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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