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Links from GEO DataSets

Items: 11

1.

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
2.
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
3.

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
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.

TRIM24 suppresses development of spontaneous hepatic lipid accumulation and hepatocellular carcinoma in mice

(Submitter supplied) Purpose: berrantly high expression of TRIM24 occurs in human cancers, including hepatocellular carcinoma. In contrast, TRIM24 in the mouse is reportedly a liver-specific tumor suppressor. To address this dichotomy and uncover direct regulatory functions of TRIM24 in vivo, we developed a new mouse model that lacks expression of all Trim24 isoforms, as the previous model expresses normal levels of Trim24 lacking only exon 4. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE61117
ID:
200061117
8.

Functional TRIM24 degraders via conjugation of ineffectual bromodomain and VHL ligands [RNA-Seq 2]

(Submitter supplied) The addressable pocket of a target protein is often not functionally relevant. This is particularly true for multidomain gene regulatory proteins, such as the bromodomain-containing transcriptional regulator TRIM24. TRIM24 has been posited as a dependency in numerous human cancers, yet potent and selective ligands for the TRIM24 bromodomain do not exert effective anti-proliferative responses. We therefore repositioned these probes as targeting features for heterobifunctional protein degraders.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
45 Samples
Download data: TXT
Series
Accession:
GSE106579
ID:
200106579
9.

Functional TRIM24 degraders via conjugation of ineffectual bromodomain and VHL ligands

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
69 Samples
Download data: WIG
Series
Accession:
GSE100573
ID:
200100573
10.

Functional TRIM24 degraders via conjugation of ineffectual bromodomain and VHL ligands [RNA-seq]

(Submitter supplied) The addressable pocket of a target protein is often not functionally relevant. This is particularly true for multidomain gene regulatory proteins, such as the bromodomain-containing transcriptional regulator TRIM24. TRIM24 has been posited as a dependency in numerous human cancers, yet potent and selective ligands for the TRIM24 bromodomain do not exert effective anti-proliferative responses. We therefore repositioned these probes as targeting features for heterobifunctional protein degraders.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: TXT
Series
Accession:
GSE100572
ID:
200100572
11.

Functional TRIM24 degraders via conjugation of ineffectual bromodomain and VHL ligands [ChIP-seq]

(Submitter supplied) The addressable pocket of a target protein is often not functionally relevant. This is particularly true for multidomain gene regulatory proteins, such as the bromodomain-containing transcriptional regulator TRIM24. TRIM24 has been posited as a dependency in numerous human cancers, yet potent and selective ligands for the TRIM24 bromodomain do not exert effective anti-proliferative responses. We therefore repositioned these probes as targeting features for heterobifunctional protein degraders.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: WIG
Series
Accession:
GSE100571
ID:
200100571
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