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Links from GEO DataSets

Items: 10

1.

Negative regulation of the IFN/STAT signaling pathway by the Trim24 tumor suppressor protein through Rara inhibition

(Submitter supplied) Recent genetic studies in mice have established a key role for the nuclear receptor coregulator Trim24 in liver tumor suppression and provided evidence that Trim24 suppresses hepatocarcinogenesis by inhibiting retinoic acid receptor alpha (Rara)-dependent transcription and cell proliferation. However, it is unknown which downstream targets of Rara regulated by Trim24 are critical for tumorigenesis. We report here that loss of Trim24 results in the overexpression of interferon (IFN)/STAT pathway genes in the liver, a process that occurs early in tumorigenesis and is more pronounced in tumors, despite the enhanced expression, late in the disease, of negative regulators such as Usp18, Socs1 and Socs2. Remarkably, Rara haplodeficiency, which was previously shown to suppress tumor development in Trim24-/- mice, also suppresses overexpression of the IFN/STAT pathway, thus providing evidence for a cross-pathway control that may be relevant to the transformation process. Biochemical studies revealed that Trim24 binds to the retinoic acid (RA)-responsive element in the Stat1 promoter in a RA-dependent manner and represses RA-induced transcription from this promoter. Together, these results identify Trim24 as a novel regulator of the IFN/STAT pathway and indicate that Trim24-mediated repression of the IFN/STAT signaling through Rara inhibition may play a critical role in preventing liver cancer.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
22 Samples
Download data: CEL, CHP
Series
Accession:
GSE19675
ID:
200019675
2.

Expression data from spontaneous liver tumors of Trim24/TIF1a-null mice.

(Submitter supplied) The transcriptional coregulator Trim24 (formerly known as TIF1a) functions in mice as a liver-specific tumor suppressor. Mice carrying a null mutation in the Trim24 gene all develop hepatocellular carcinoma (HCC). We used microarrays to identify the alterations in gene expression patterns associated with loss of Trim24 and consequent HCC development. Keywords: normal-tumor comparison
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3087
Platform:
GPL1261
10 Samples
Download data: CEL, CHP, EXP
Series
Accession:
GSE9012
ID:
200009012
3.
Full record GDS3087

Trim24 deficient hepatocellular carcinoma tumors

Analysis of hepatocellular carcinoma (HCC) tumors from animals lacking Trim24 (Tif1alpha). Trim24 is a ligand-dependent nuclear receptor transcriptional co-regulator. Animals lacking Trim24 develop HCC. Results provide insight into the potential role of Trim24 as a liver-specific tumor suppressor.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 disease state sets
Platform:
GPL1261
Series:
GSE9012
10 Samples
Download data: CEL, CHP, EXP
DataSet
Accession:
GDS3087
ID:
3087
4.

VL30 retro-transposons are TRIM24-repressed enhancers that generate non-coding RNA to regulate gene expression in mouse hepatocytes.

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11002
6 Samples
Download data: WIG
Series
Accession:
GSE39853
ID:
200039853
5.

VL30 retro-transposons are TRIM24-repressed enhancers that generate non-coding RNA to regulate gene expression in mouse hepatocytes. [ChIP-Seq]

(Submitter supplied) TRIM24 and TRIM33 interact to form a corepressor complex that suppresses murine hepatocellular carcinoma (HCC). TRIM24 and TRIM33 cooperatively repress retinoic acid receptor dependent activity of VL30 retro-transposons in hepatocytes in vivo. In TRIM24 knockout hepatocytes, VL30 long terminal repeats (LTRs) generate enhancer (e)RNAs and act as surrogate promoter and enhancer elements deregulating expression of neighbouring genes. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11002
4 Samples
Download data: WIG
Series
Accession:
GSE39852
ID:
200039852
6.

VL30 retro-transposons are TRIM24-repressed enhancers that generate non-coding RNA to regulate gene expression in mouse hepatocytes. [RNA-Seq]

(Submitter supplied) TRIM24 and TRIM33 interact to form a corepressor complex that suppresses murine hepatocellular carcinoma (HCC). TRIM24 and TRIM33 cooperatively repress retinoic acid receptor dependent activity of VL30 retro-transposons in hepatocytes in vivo. In TRIM24 knockout hepatocytes, VL30 long terminal repeats (LTRs) generate enhancer (e)RNAs and act as surrogate promoter and enhancer elements deregulating expression of neighbouring genes. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11002
2 Samples
Download data: WIG
Series
Accession:
GSE39851
ID:
200039851
7.

Cistrome profiles of Retinoids x Receptor alpha (RXRα) , Retinoic Acid Receptor alpha (RARα), and Retinoic Acid Receptor beta (RARβ) in livers of mice treated by control and retionic acid-containing diet

(Submitter supplied) Comparison between ChIP-Seq data of RARα and RARβ, between RAR and RXR, as well as between control and retinoic acid-treatment for each investigated nuclear receptors.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
7 Samples
Download data: BED
Series
Accession:
GSE53736
ID:
200053736
8.

Gene expression data of untreated and RA-treated wild type and RXRα-deficient mice liver

(Submitter supplied) Our project focuses on retinoic acid (RA) effect on hepatic lipid homeostasis. Even though RA has more than one receptor including retinoids x receptor (RXR) and retinoic acid receptor (RAR), most probably, RA effect on lipid homeostasis is mediated by RXR and its partners such as PXR, FXR, and PPAR. So we treated the wild type and RXRα-knockout mice by retinoic acid to check the global gene expression especially for lipid homeostasis genes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
12 Samples
Download data: CEL
Series
Accession:
GSE50028
ID:
200050028
9.

Expression data from wild-type bone marrow-derived macrophages non-treated (NT1 and NT2) or stimulated for 12 h with VSV virus(VSV1 and VSV2)

(Submitter supplied) We conducted gene expression profile analysis by using wild-type bone marrow-derived macrophages. Heatmap revealed the most prominent different expression of genes encoding E3 ligases or DUBs altered in macrophages upon VSV stimulation were associated with typeⅠIFN genes.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
4 Samples
Download data: TXT
Series
Accession:
GSE136363
ID:
200136363
10.

The oncofusion protein FUS-ERG targets key hematopoietic regulators and modulates the all-trans retinoic acid signaling pathway in t(16;21) acute myeloid leukemia

(Submitter supplied) Fusion proteins involving the ETS factor ERG have been associated with multiple cancers such as Ewing's sarcoma and prostate cancer. In acute myeloid leukemias harboring t(16;21) another ERG fusion protein is expressed, FUS-ERG. Here, we found that this FUS-ERG oncofusion protein acts in the context of a heptad of proteins (ERG, FLI1, GATA2, LYL1, LNMO2, RUNX1 and TAL1) central to proper expression of genes involved in maintaining a stem cell hematopoietic phenotype. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL10999 GPL11154
20 Samples
Download data: WIG
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