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.
NF-κB functions in tumor initiation by suppressing the surveillance of both innate and adaptive immune cells.
Specimen part
View SamplesMultiple 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.
IKKα-mediated signaling circuitry regulates early B lymphopoiesis during hematopoiesis.
Specimen part
View SamplesTo 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.
Mineralocorticoid receptors are present in skeletal muscle and represent a potential therapeutic target.
Sex
View SamplesTo identify the gene expression differences in skeletal muscles resulting from treatment of dystrophic mice with spironolactone plus lisinopril
Mineralocorticoid receptors are present in skeletal muscle and represent a potential therapeutic target.
Sex, Age, Treatment
View SamplesDuring neonatal development, skeletal muscle grows dramatically by myonuclei accretion to existing fibers and hypertophic growth of fibers with protein synthesis.
An NF-κB--EphrinA5-Dependent Communication between NG2(+) Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates.
Specimen part
View SamplesDuring 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.
An NF-κB--EphrinA5-Dependent Communication between NG2(+) Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates.
Specimen part, Subject
View SamplesRectus 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.
Using transcriptomics to identify and validate novel biomarkers of human skeletal muscle cancer cachexia.
Sex, Age, Specimen part, Disease
View SamplesWe 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
NF-κB regulates GDF-15 to suppress macrophage surveillance during early tumor development.
Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
NF-κB inhibition rescues cardiac function by remodeling calcium genes in a Duchenne muscular dystrophy model.
Age
View SamplesWe 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.
NF-κB inhibition rescues cardiac function by remodeling calcium genes in a Duchenne muscular dystrophy model.
Age
View Samples