CRABP2 potently suppresses carcinoma cell growth, yet the mechanism(s) that underlie this activity remain incompletely understood. Two distinct functions are known for CRABP2: 1) the classical function of this protein is to directly deliver retinoic acid (RA) to the nuclear retinoic-acid receptorthereby activate gene expression, and 2) in the absence of RA, CRABP2 directly binds to the RNA-binding and stabilizing protein, HuR, and markedly strengthens its interactions with target mRNAs.
Cellular retinoic acid-binding protein 2 inhibits tumor growth by two distinct mechanisms.
Specimen part, Cell line
View SamplesThe aim of the present study was to compare, on a statistical basis, the performance of different microarray platforms to detect differences in gene expression in a realistic and challenging biological setting. Gene expression profiles in the hippocampus of five wild-type and five transgenic C-doublecortin-like kinase mice were evaluated with five microarray platforms: Applied Biosystems, Affymetrix, Agilent, Illumina and home-spotted oligonucleotide arrays. We observed considerable overlap between the different platforms, the overlap being better detectable with significance level-based ranking than with a p-value based cut-off. Confirming the qualitative agreement between platforms, Pathway analysis consistently demonstrated aberrances in GABA-ergic signalling in the transgenic mice, even though pathways were represented by only partially overlapping genes on the different platforms.
Can subtle changes in gene expression be consistently detected with different microarray platforms?
No sample metadata fields
View SamplesTranscriptomic comparison of FVB mouse strain lung Cells one week upon injecting mice intraperitoneally with either saline or Urethane. Mouse lung cell were also compared at the transcriptomic level with the mouse lung adenocarcinoma cell line FULA 1, which was established in our lab
IκB Kinase α Is Required for Development and Progression of <i>KRAS</i>-Mutant Lung Adenocarcinoma.
Specimen part, Cell line, Treatment
View SamplesWe compared different mouse cancer cell lines to identify their unique cell signatures.
Myeloid-derived interleukin-1β drives oncogenic KRAS-NF-κΒ addiction in malignant pleural effusion.
Cell line, Treatment
View SamplesWe compared different mouse cancer cell lines to identify their unique cell signatures.
<i>NRAS</i> destines tumor cells to the lungs.
Specimen part, Cell line
View SamplesWe compared different mouse cancer cell lines to identify their unique cell signatures.
Mutant KRAS promotes malignant pleural effusion formation.
Specimen part, Cell line
View SamplesWe compared different mouse cancer cell lines to identify their unique cell signatures.
Mutant KRAS promotes malignant pleural effusion formation.
Specimen part, Cell line
View SamplesWe isolated mouse epithelial trachea cells from FVB mice in order to identify their transcriptomic signature.
Mutant KRAS promotes malignant pleural effusion formation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Mast cells mediate malignant pleural effusion formation.
Specimen part, Cell line
View SamplesNave mast cells were cultured from murine bone marrow using incubation with IL-3 alone (samples 1-4) or IL-3 and KITL (samples 5-8).
Mast cells mediate malignant pleural effusion formation.
No sample metadata fields
View Samples