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Mus musculus
20 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Reversible protein acetylation provides a central mechanism for controlling gene expression and cellular signaling events. It is governed by the antagonistic commitment of two enzymes families: the histone acetyltransferases (HATs) and the histone deacetylases (HDACs). HDAC4, like its class IIa counterparts, is a potent transcriptional repressor through interactions with tissue-specific transcription factors via its N-terminal domain. Whilst the lysine deacetylase activity of the class IIa HDACs is much less potent than that of the class I enzymes, HDAC4 has been reported to influence protein deacetylation through its interaction with HDAC3.
Publication Title
HDAC4 does not act as a protein deacetylase in the postnatal murine brain in vivo.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 30 Downloadable Samples
Illumina HiSeq 2000
Description
Purpose: Transcriptome profiling (RNA-seq) to microarray to evaluate transcriptional changes in the heart of HD mouse models Methods: Heart mRNA profiles of 4-weeks-old wild-type (WT) and R6/2 transgenic; 15-weeks-old WT and R6/2 transgenic mice; 8-month-old WT and HdhQ150 knock-in mice; 22-month-old WT and HdhQ150 knock-in mice were generated by deep sequencing, in triplicate, using Illumina Hi-seq 2000. Conclusions: Our study showed that there is no major transcriptional deregulation in the heart of mouse models of HD. Overall design: Heart mRNA profiles of 4-weeks-old wild-type (WT) and R6/2 transgenic; 15-weeks-old WT and R6/2 transgenic mice; 8-month-old WT and HdhQ150 knock-in mice; 22-month-old WT and HdhQ150 knock-in mice were generated by deep sequencing, in triplicate, using Illumina Hi-seq 2000.
Publication Title
Dysfunction of the CNS-heart axis in mouse models of Huntington's disease.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 71 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
HDAC4 reduction: a novel therapeutic strategy to target cytoplasmic huntingtin and ameliorate neurodegeneration.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 37 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Histone deacetylase (HDAC) 4 is a transcriptional repressor that contains a glutamine rich domain. We hypothesised that it may be involved in the molecular pathogenesis of Huntingtons disease (HD), a protein folding neurodegenerative disorder caused by an aggregation-prone polyglutamine expansion and transcriptional dysregulation. We found that HDAC4 interacts with huntingtin in a polyglutamine-length dependent manner and co-localises with cytoplasmic inclusions. We show that HDAC4 reduction delayed cytoplasmic aggregate formation, restored Bdnf transcript levels and rescued neuronal and cortico-striatal synaptic function in HD mouse models. This was accompanied by an improvement in motor co-ordination, neurological phenotypes and increased lifespan. Surprisingly, HDAC4 reduction had no effect on global transcriptional dysfunction and did not modulate nuclear huntingtin aggregation. Our results define a crucial role for cytoplasmic aggregation in the molecular pathology of HD. HDAC4 reduction presents a novel strategy for targeting huntingtin aggregation which may be amenable to small molecule therapeutics.
Publication Title
HDAC4 reduction: a novel therapeutic strategy to target cytoplasmic huntingtin and ameliorate neurodegeneration.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 34 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Histone deacetylase (HDAC) 4 is a transcriptional repressor that contains a glutamine rich domain. We hypothesised that it may be involved in the molecular pathogenesis of Huntingtons disease (HD), a protein folding neurodegenerative disorder caused by an aggregation-prone polyglutamine expansion and transcriptional dysregulation. We found that HDAC4 interacts with huntingtin in a polyglutamine-length dependent manner and co-localises with cytoplasmic inclusions. We show that HDAC4 reduction delayed cytoplasmic aggregate formation, restored Bdnf transcript levels and rescued neuronal and cortico-striatal synaptic function in HD mouse models. This was accompanied by an improvement in motor co-ordination, neurological phenotypes and increased lifespan. Surprisingly, HDAC4 reduction had no effect on global transcriptional dysfunction and did not modulate nuclear huntingtin aggregation. Our results define a crucial role for cytoplasmic aggregation in the molecular pathology of HD. HDAC4 reduction presents a novel strategy for targeting huntingtin aggregation which may be amenable to small molecule therapeutics.
Publication Title
HDAC4 reduction: a novel therapeutic strategy to target cytoplasmic huntingtin and ameliorate neurodegeneration.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfngs roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown altered Notch activation, decreased tumor sphere formation in vitro, and reduced tumor growth in xenograft model. To identify the potential downstream targets of Mfng during CLBC tumorigenesis, we compared the gene expression profiles between xenografts tumor derived from of MDA-MB231 cells carrying Mfng shRNA and the control vector. Mfng, a modulator of Notch signaling, is highly expressed in human claudin-low breast cancer (CLBC). To determine Mfngs roles in CLBC pathogenesis,we knocked down Mfng in a CLBC cell line MDA-MB231, and found that Mfng knockdown caused alteration in Notch activation, associated with decreased tumor sphere formation in vitro, as well as reduced tumor growth in xenograft model. We intend to compare gene expression profiles between xenografts of MDA-MB231 cells carrying Mfng shRNA and the control vector. This project seeks to identify potential downstream targets of Mfng in CLBC.
Publication Title
Manic fringe promotes a claudin-low breast cancer phenotype through notch-mediated PIK3CG induction.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Decidualization is a critical process for embryo implatation during which uterine stromal fibroblasts are transformed into large, epithelioid-like decidual cell. NOTCH1 is recepotor of Notch signaling that plays important roles for cell-cell communication, which involves gene regulatory mechanisms that control multiple cellular differentiation processes during embryonic and adult life.
Publication Title
Decreased Notch pathway signaling in the endometrium of women with endometriosis impairs decidualization.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
In this study, we aim to identify candidate biomarkers which may be useful as surrogate indicators of toxicity for pre-clinical development of panPPAR-agonist drug candidates. Gene expression microarray, histopathology and clinical chemistry data were generated from liver, heart, kidney and skeletal muscles of three groups of mice administered with three different dosages of an experimental pan-peroxisome proliferator-activated receptor (pan-PPAR) agonist, PPM-201, for 14 days. The histopathology and clinical chemistry data were compared with the gene expression analysis and candidate biomarker genes were identified.
Publication Title
Simultaneous non-negative matrix factorization for multiple large scale gene expression datasets in toxicology.
Sample Metadata Fields
Specimen part, Treatment
View Samples
GSE2124- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
treatment of mesenteric lymph nodes with soluble lymphotoxin-beta receptor for 0,1,2,3,27 and 35 days
Publication Title
Lymphotoxin-beta receptor-dependent genes in lymph node and follicular dendritic cell transcriptomes.
Sample Metadata Fields
No sample metadata fields
View Samples GSE2123- Mus musculus
- 14 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Comparison of follicular dendritic cell-enriched versus -depleted splenocytes
Publication Title
Lymphotoxin-beta receptor-dependent genes in lymph node and follicular dendritic cell transcriptomes.
Sample Metadata Fields
No sample metadata fields
View Samples