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accession-icon GSE73222
Lung adenocarcinoma distally rewires hepatic circadian homeostasis
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Gene expression was performed in WT and tumor-bearing (TB) mice to determine the effects of a lung tumor on circadian clock of the liver.

Publication Title

Lung Adenocarcinoma Distally Rewires Hepatic Circadian Homeostasis.

Sample Metadata Fields

Specimen part, Disease

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accession-icon SRP153814
Dissecting the autonomy of the liver circadian clock
  • organism-icon Mus musculus
  • sample-icon 54 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The mammalian circadian clock system is made up of individual cell and tissue clocks that function as a coherent network, however it remains unclear which rhythmic functions of the liver clock are autonomous or rely on clocks in other tissues. Here, using mice which only have a functioning liver clock, we investigate the autonomous vs non-autonomous reatures of the liver clock and diurnal rhythmicity in the liver Overall design: 8-12 week-old, female WT, KO and Liver-RE BMAL1-stop-FL mice (see referenced paper for details) were fed ad libitum normal chow under 12hr light/ 12hr dark schedule. Livers were harvested every 4 hours over the circadian cycle at ZT0, 4, 8, 12, 16, 20 (n=3 per time point per group). Total RNA was extracted and used for RNA-seq.

Publication Title

Defining the Independence of the Liver Circadian Clock.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP126336
Fasting Imparts a Switch to Alternative Circadian Transcriptional Pathways in Liver and Muscle
  • organism-icon Mus musculus
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

The circadian gene expression in peripheral tissue displays rhythmicity which is driven by the circadian clock and feeding-fasting cycle in mammals. In this study, circadian transcriptome was performed to investigate how fasting influences circadian gene regulation. Overall design: 8-week-old, male C57BL/6 mice were subjected to 24-hr fasting (FAST) or to ad libitum normal chow feeding (FED) under 12hr light/ 12hr dark schedule. Liver and gastrocnemius muscle were harvested every 4 hours over the circadian cycle at ZT0, 4, 8, 12, 16, 20 (n=3 per time point per group). Total RNA was extracted from liver and gastrocnemius muscle, and used for RNA-seq.

Publication Title

Fasting Imparts a Switch to Alternative Daily Pathways in Liver and Muscle.

Sample Metadata Fields

Age, Cell line, Subject

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accession-icon SRP148999
Light can synchronise peripheral clocks autonomously from each other [darkness experiment (DD)]
  • organism-icon Mus musculus
  • sample-icon 70 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Organisms have adapted to the changing environmental conditions within the 24h cycle of the day by temporally segregating tissue physiology to the optimal time of the day. On the cellular level temporal segregation of physiological processes is established by the circadian clock, a Bmal1 dependent transcriptional oscillator network. The circadian clocks within individual cells of a tissue are synchronised by environmental signals, mainly light, in order to reach temporally segregated physiology on the tissue level. However, how light mediated synchronisation of peripheral tissue clocks is achieved mechanistically and whether circadian clocks in different organs are autonomous or interact with each other to achieve rhythmicity is unknown. Here we report that light can synchronise core circadian clocks in two peripheral tissues, the epidermis and liver hepatocytes, even in the complete absence of functional clocks in any other tissue within the whole organism. On the other hand, tissue extrinsic circadian clock rhythmicity is necessary to retain rhythmicity of the epidermal clock in the absence of light, proving for the first time that the circadian clockwork acts as a memory of time for the synchronisation of peripheral clocks in the absence of external entrainment signals. Furthermore, we find that tissue intrinsic Bmal1 is an important regulator of the epidermal differentiation process whose deregulation leads to a premature aging like phenotype of the epidermis. Thus, our results establish a new model for the segregation of peripheral tissue physiology whereby the synchronisation of peripheral clocks is acquired by the interaction of a light dependent but circadian clock independent pathway with circadian clockwork dependent cues. Overall design: Determining the epidermal circadian transcriptome in the presence or absence of non-epidermal clocks after 6-7 days in complete darkness (DD).

Publication Title

BMAL1-Driven Tissue Clocks Respond Independently to Light to Maintain Homeostasis.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP149357
Light can synchronise peripheral clocks autonomously from each other
  • organism-icon Mus musculus
  • sample-icon 72 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Organisms have adapted to the changing environmental conditions within the 24h cycle of the day by temporally segregating tissue physiology to the optimal time of the day. On the cellular level temporal segregation of physiological processes is established by the circadian clock, a Bmal1 dependent transcriptional oscillator network. The circadian clocks within individual cells of a tissue are synchronised by environmental signals, mainly light, in order to reach temporally segregated physiology on the tissue level. However, how light mediated synchronisation of peripheral tissue clocks is achieved mechanistically and whether circadian clocks in different organs are autonomous or interact with each other to achieve rhythmicity is unknown. Here we report that light can synchronise core circadian clocks in two peripheral tissues, the epidermis and liver hepatocytes, even in the complete absence of functional clocks in any other tissue within the whole organism. On the other hand, tissue extrinsic circadian clock rhythmicity is necessary to retain rhythmicity of the epidermal clock in the absence of light, proving for the first time that the circadian clockwork acts as a memory of time for the synchronisation of peripheral clocks in the absence of external entrainment signals. Furthermore, we find that tissue intrinsic Bmal1 is an important regulator of the epidermal differentiation process whose deregulation leads to a premature aging like phenotype of the epidermis. Thus, our results establish a new model for the segregation of peripheral tissue physiology whereby the synchronisation of peripheral clocks is acquired by the interaction of a light dependent but circadian clock independent pathway with circadian clockwork dependent cues. Overall design: Determining the epidermal circadian transcriptome in the presence or absence of non-epidermal clocks under light entrainment (LD).

Publication Title

BMAL1-Driven Tissue Clocks Respond Independently to Light to Maintain Homeostasis.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

View Samples
accession-icon SRP140471
A Zebrafish Acromegaly Model Elevates DNA Damage and Impairs DNA Repair Pathways
  • organism-icon Danio rerio
  • sample-icon 27 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Acromegaly is a pathological condition due to excess growth hormone (GH) secretion. Acromegaly patients exhibit a deterioration of health and many associated complications, such as cardiovascular issues, arthritis, kidney diseases, muscular weakness, and colon cancer. Since these complications are generalized throughout the body, we investigated the effect of GH excess on cellular integrity. Here, we established stable acromegaly model zebrafish lines that overexpress tilapia GH and the red fluorescence protein (RFP) reporter gene for tracking GH gene expression throughout generations, and performed RNA-Seq data analysis from different organs. Intriguingly, heatmap and Expression2Kinases (X2K) analysis revealed the enrichment of DNA damage markers in various organs. Moreover, H2A.X immunostaining analysis in acromegaly zebrafish larvae and the adult acromegaly model brain and muscle showed a robust increase in the number of DNA-damaged cells. Using Gene Set Enrichment Analysis (GSEA), we found that the acromegaly zebrafish model had impaired DNA repair pathways in the liver, such as double-strand break (DSB), homologous recombination repair (HRR), non-homologous end joining (NHEJ), nucleotide excision repair (NER), and translesion synthesis (TLS). Interestingly, the impairment of DNA repair was even more prominent in acromegaly model than in aged zebrafish (three years old). Thus, our study demonstrates that affection of cellular integrity is characteristic of acromegaly Overall design: Total mRNA obtained from 1-years old acromegaly zebrafish model muscle, brain, kidney, liver and 3-day old larvae compared to wild-type (WT) zebrafish were generated by deep sequencing using Illumina.

Publication Title

An Acromegaly Disease Zebrafish Model Reveals Decline in Body Stem Cell Number along with Signs of Premature Aging.

Sample Metadata Fields

Age, Specimen part, Subject

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accession-icon GSE44116
Cytosolic Fe-S cluster assembly-deficient mutant, nar1 and nbp35 mutant seedling
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Expression profiling of two-weeks-old wild type, nar1-4/- and nbp35-3/- mutant seedlings. The cytosolic Fe -S cluster assembly pathway is involved in cytosolic and nucleus Fe-S protein maturation.

Publication Title

The role of Arabidopsis thaliana NAR1, a cytosolic iron-sulfur cluster assembly component, in gametophytic gene expression and oxidative stress responses in vegetative tissue.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE11119
SOL2 mutation affect gene expresstion at root apex
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Analysis of sol2 mutant. SOL2 protein is a receptor-like kinase

Publication Title

The receptor-like kinase SOL2 mediates CLE signaling in Arabidopsis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE140855
Microarray of HEK293-PIGS-KO and HEK293-PIGS-UBE2J1-DKO cells.
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Clariom S Human array (clariomshuman)

Description

Transcriptome analysis of total RNA samples from HEK293-PIGS-KO and HEK293-PIGS-UBE2J1-DKO cells. To check whether KO of UBE2J1 upregulates genes of GPI biosthesis pathway, we used microarrays to analyze gene expression change by KO of UBE2J1 and comfirmed that known GPI pathway genes are not changed by ERAD-deficiency.

Publication Title

Cross-talks of glycosylphosphatidylinositol biosynthesis with glycosphingolipid biosynthesis and ER-associated degradation.

Sample Metadata Fields

Cell line

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accession-icon GSE16494
Expression profiling MOLT-4 treated with MABL
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Analysis of MOLT-4 cells at various time points up to 6 hours following treatment with mouse anti-CD47 antibody (MABL) and goat anti-mouse IgG (GAM) as the crosslinker of MABL. MABL induces apoptosis in CD47-positive MOLT-4 cells. Cell death signals via CD47 ligation were analyzed by using Affymetrix Human Genome U133A microarray.

Publication Title

A new disulfide-linked dimer of a single-chain antibody fragment against human CD47 induces apoptosis in lymphoid malignant cells via the hypoxia inducible factor-1α pathway.

Sample Metadata Fields

Cell line, Time

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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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