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accession-icon SRP182110
Oocyte-specific deletion of Mitofusin1 causes female infertility and accelerated follicular depletion
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We performed RNAseq analysis to determine the effect of MFN1 deletion on oocyte global gene expression profile. RNAseq revealed a total of 982 genes were significantly differentially expressed (p<0.05) in Mfn1-/- oocytes compared to WT (654 up-regulated and 337 down-regulated). Pathway analysis indicated significant over-representation of elements involved in regulation of ceramide biosynthesis, death receptor signaling and adherens junction signaling. Differential expression of these genes (Bad, G2e3, Cdh17 and Myh2) was also confirmed by qRT-PCR.Our findings provide new insight into the role of MFN1 in the oocytes, and may help understand the potential mechanism of infertility and reproductive aging associated with MFN1-deficiency. Overall design: Secondary follicle-enclosed oocytes were collected from 8-week-old Mfn1-/- and WT mice (n=3 for each group) and 5 oocytes from each group were pooled for RNA sequencing analysis.

Publication Title

Mitofusin 1 is required for female fertility and to maintain ovarian follicular reserve.

Sample Metadata Fields

Cell line, Subject

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accession-icon SRP078500
ARID1A-mutated ovarian cancers depend on HDAC6 activity
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

ARID1A, encoding a subunit of the SWI/SNF chromatin remodeling complex, is the most mutated epigenetic regulator in human cancers. ARID1A and TP53 mutations are typically mutually exclusive. Therapeutic approaches that correlate with ARID1A mutational status remain a challenge. Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers. Inhibition of HDAC6 activity using a clinically applicable small molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated ovarian tumors. This correlated with the suppression of growth and dissemination of ARID1A-mutated, but not wild-type, tumors. The dependence on HDAC6 activity in ARID1A-mutated cells correlated with a direct transcriptional repression of HDAC6 by ARID1A. HDAC6 inhibition selectively promoted apoptosis of ARID1A-mutated cells. HDAC6 directly deacetylated the Lysine 120 residue of p53, a pro-apoptotic post-translational modification. Thus, ARID1A mutation inactivates p53' apoptotic function by upregulating HDAC6. These results indicate that pharmacological inhibition of HDAC6 is a novel therapeutic strategy involving ARID1A-mutation Overall design: RNA-seq transcription profiling of samples with altered HDAC6 activity

Publication Title

ARID1A-mutated ovarian cancers depend on HDAC6 activity.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon SRP078244
Recognition memory-induced gene expression in the perirhinal cortex: a transcriptomics analysis.
  • organism-icon Rattus norvegicus
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

It is possible to identify the key genes and pathways involved in specific physiological processes using transcriptome analyses. However, these powerful new deep sequencing-based methods have rarely been applied to studies of memory function. We used the bow-tie maze to train rats by exposing them to highly familiar objects or to novel objects. Total RNA sequencing was then used to compare the transcriptome of the perirhinal cortices of naïve control rats and rats exposed to novel and familiar stimuli. Differentially expressed genes were identified between group Novel and group Familiar rats and these included genes coding for transcription factors and extracellular matrix-related proteins. Moreover, differences in alternative splicing were also detected between the two groups. To conclude, this study shows that RNA sequencing can be used as a tool to identify differences in gene expression in behaving animals undergoing the same task but encountering different exposures. Overall design: RNA profiles of perirhinal cortex from rats exposed to novel objects (n=5) or familiar objects (n=5) in a recognition memory task were investigated using the Ion Proton System. Controls were naïve rats that had not undergone any behavioural testing (n=4).

Publication Title

Recognition memory-induced gene expression in the perirhinal cortex: A transcriptomic analysis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE11826
Identifying alterations of gene expression induced by two teratogenic agents which induce a similar phenotype
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

Samples used for hybridization consisted of non-pooled (NP) RNA extracts from 8 groups in each of two time periods after drug administration: oil vehicle treated control embryonic limb bud mesoderm and ectoderm, phosphate buffered saline vehicle control embryonic limb bud mesoderm and ectoderm, acetazolamide treated embryonic limb bud mesoderm and ectoderm, and cadmium sulfate treated embryonic limb bud mesoderm and ectoderm. Forty-eight hybridization experiments were on non-pooled (NP) individual RNA extracts.

Publication Title

Microarray analysis of murine limb bud ectoderm and mesoderm after exposure to cadmium or acetazolamide.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3414
Immune Response to Nippostrongylus brasiliensis in the mouse lung
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The goal of this experiment was to examine the innate immune response to helminth infection in the lung. Hookworms (like many other helminths) use an obligate migration pathway through the lung. Their infection has been characterized in the gut in detail, but early immune responses in the lung have not been fully characterized.

Publication Title

Innate immune responses to lung-stage helminth infection induce alternatively activated alveolar macrophages.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE57115
Placental gene expression in intestinal nematode-infected and protein-deficient mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Protein deficiency and intestinal parasite infection during pregnancy impair fetal growth through passage of signals from the maternal environment which signal impairment of fetal growth. The placenta is an important regulator of the transfer of these signals through differential expression of key placental genes. We used microarrays to examine placental gene expression responses to maternal protein deficiency (6% vs. 24% protein) and Heligmosomoides bakeri infection.

Publication Title

Expression of growth-related genes in the mouse placenta is influenced by interactions between intestinal nematode (Heligmosomoides bakeri) infection and dietary protein deficiency.

Sample Metadata Fields

Specimen part

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accession-icon GSE19984
Gene expression analysis of Drosophila melanogaster taste tissue
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

To uncover novel molecules involved in taste detection, we performed a microarray-based screen for genes enriched in taste neurons. Proboscis RNA from flies homozygous for a recessive poxn null mutation was compared to RNA from heterozygous controls. Poxn mutants have a transformation of labellar gustatory chemosensory bristles into mechanosensory bristles and therefore lack most or all taste neurons.

Publication Title

The molecular basis for water taste in Drosophila.

Sample Metadata Fields

Sex

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accession-icon GSE36119
Global gene expression change in the cerebellum of Niemann-Pick disease type C mice with deletion of Ccl3 or Purkinje neuron-specific NPC1 rescue
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Macrophage inflammatory protein 1alpha/CCL3 protein is a known pro-inflammatory cytokine that can mediate chemotaxis of monocytes and promote cell degranulation. Ccl3 gene expression is elevated in the CNS and visceral tissue of many lysosomal storage disorders. The deletion of Ccl3 in a mouse model of Sandhoff disease was reported to result in reduced monocyte-associated pathology in the brain, delayed neurodegeneration, and prolonged health. However, deletion of Ccl3 in a mouse model of Niemann-Pick C disease was dentrimental or neutral instead of beneficial. Prevention of neuronal loss was instead mediated by providing NPC1 to neurons.

Publication Title

Neuronal and epithelial cell rescue resolves chronic systemic inflammation in the lipid storage disorder Niemann-Pick C.

Sample Metadata Fields

Specimen part

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accession-icon GSE63659
Transcriptomic Changes in TGF-1 Differentiated and PGE2 Dedifferentiated Myofibroblasts
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

These data show that the genes that distinguish myofibroblasts from fibroblasts are myriad, and that some genes not traditionally associated with myofibroblast differentiation may serve as novel therapeutic targets for fibrosing disorders.

Publication Title

Reversal of the Transcriptome by Prostaglandin E2 during Myofibroblast Dedifferentiation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE2560
Transcriptomes analysis of mouse developing forelimb and hindlimb autopods
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Transcriptomes of mouse embryonic autopods were generated detecting expression of approximately 26179 transcripts in the developing forelimb or hindlimb autopods, representing about 58 % of the probe sets on MOE-430 A/B GeneChip. Three biological replicate array experiments were finished for each condition and MAS5.0 signal were used to do data analysis. Forty-four transcripts with expression differences higher than 2-fold were detected(T test, P<0.05), including Tbx4, Tbx5, Hoxc10 and Pitx1 which were previously shown to be differentially expressed in developing forelimb and hindlimb bud by in situ hybridization and SAGE study (Margulies 2001). RTPCR and in situ experiments confirmed several top differentially expressed genes which were newly discovered by our experiments. Vast amount of transcripts and its family members such as Bmp, Fgf, Epha, Wnt, T-box and Hox families detected to be highly expressed or differentially expressed in developing autopods, suggesting that the complexity of transcriptomes of developing autopods and dynamic differential expression and differential combinations of gene expression signals in the developing limb tissue contributes to differences in forelimb versus hindlimb patterning. The differentially expressed genes are the essential factors for morphological diversification of developing limb structures.

Publication Title

Transcriptome analysis of the murine forelimb and hindlimb autopod.

Sample Metadata Fields

No sample metadata fields

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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