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accession-icon GSE37165
Gene expression data from time course of fin regeneration in Danio rerio
  • organism-icon Danio rerio
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE37164
Gene expression data from time course of fin regeneration in Danio rerio (part 2)
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon GSE37163
Gene expression data from time course of fin regeneration in Danio rerio (part 1)
  • organism-icon Danio rerio
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Olsen et al (2010) have shown that induced Diabetes mellitus (DM) in adult Zebrafish results in an impairment of tissue regeneration as monitored by caudal fin regeneration. In those studies, streptozocin was used to induce hyperglycemia in adult zebrafish, and then, following streptozocin withdrawal, a recovery phase was allowed to re-establish euglycemia, due to pancreatic b-cell regeneration. DM-associated impaired fin regeneration continued indefinitely in the metabolic memory state (MM); allowing for subsequent molecular analysis of the underlying mechanisms of MM. This study focuses on elucidating the molecular basis explaining DM-associated impaired fin regeneration and why it persists into the MM state. The analysis of microarray data indicated that of the 14,900 transcripts analyzed, aberrant expression of 71 genes relating to tissue developmental and regeneration processes were identified in DM fish and the aberrant expression of these 71 genes persisted into the MM state. Key regulatory genes of major signal transduction pathways were identified among this group of 71; and therefore, these findings provide a possible explanation for how hyperglycemia induces impaired fin regeneration and why it continues into the MM state.

Publication Title

Impaired tissue regeneration corresponds with altered expression of developmental genes that persists in the metabolic memory state of diabetic zebrafish.

Sample Metadata Fields

Specimen part, Disease, Disease stage

View Samples
accession-icon SRP072732
Microglia development follows a stepwise program to regulate brain homeostasis - RNA seq
  • organism-icon Mus musculus
  • sample-icon 83 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Microglia play important roles in life-long brain maintenance and in pathology, but are also crucial in the developing central nervous system; yet their regulatory dynamics during development have not been fully elucidated. Genome-wide chromatin and expression profiling coupled with single-cell transcriptomic analysis throughout development reveal that microglia undergo three temporal developmental stages in synchrony with the brain: early, pre-, and adult microglia, which are under the control of distinct regulatory circuits. Knockout of the transcription factor MafB caused disruption of homeostasis in adulthood and increased inflammation. Environmental perturbations, such as the microbiome or prenatal immune activation, led to dysregulation of the developmental program, particularly in terms of inflammation. Together, our work identifies a stepwise developmental program of microglia integrating immune response pathways that may be associated with several neurodevelopmental disorders. Overall design: Yolk sac progenitors (CD45+CD11B+CX3CR1-GFP+), microglia from early brain (CD45+CD11B+CX3CR1-GFP+), and microglia from later stages (CD45intCD11BintCX3CR1-GFP+) were isolated from CX3CR1+ C57BL/6J mice or microglia from perturbation models (CD45intCD11Bint) from mice of C57BL/6J background

Publication Title

Microglia development follows a stepwise program to regulate brain homeostasis.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

View Samples
accession-icon GSE42781
A Splice Variant of HER2 Activates Key Signaling Cascades and Evokes Mammary Tumors and Metastases
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The Epidermal Growth Factor Receptor 2 (ERBB2 or HER2) is amplified and overexpressed in approximately 20% of invasive breast cancers and is associated with metastasis and poor prognosis. Here we describe the role of a constitutively active splice variant of HER2 (Delta-HER2) in human mammary epithelial cells. Overexpression of Delta-HER2 in human mammary cells decreased apoptosis and increased proliferation and expression of epithelial-to-mesenchymal markers. It also induced invasion in three-dimensional cultures and promoted tumorigenicity and metastasis in vivo. In contrast, similar overexpression of wild-type HER2 failed to evoke the same effects. Unbiased protein-tyrosine phosphorylation profiling revealed a significant increase in phosphorylation of several key signaling proteins upon Delta-HER2 expression, some of which not previously shown to belong to the HER2 pathway. In addition, microarray analysis revealed the expression of a set of genes specifically associated with Delta-HER2 expression. We found those genes to be highly expressed in ER-negative, high grade and metastatic primary breast tumors. Altogether, these results provide new insights into the function of a tumorigenic splice variant of HER2 and the signaling cascade deriving from its activity

Publication Title

Mammary tumor formation and metastasis evoked by a HER2 splice variant.

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE34948
Expression data from three endothelial cell lines derived from murine embryonic stem cells expressing VE-cadherin, N-cadherin or both
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Endothelial cells (ECs) express two members of the cadherin family, VE- and N-cadherin. While VE-cadherin induces EC homotypic adhesion, N-cadherin function in ECs remains largely unknown. EC-specific inactivation of either VE- or N-cadherin leads to early foetal lethality suggesting that these cadherins play a non-redundant role in vascular development.

Publication Title

Overlapping and divergent signaling pathways of N-cadherin and VE-cadherin in endothelial cells.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP089884
Single cell RNA sequencing analysis of bacterial lipoprotein-induced polyploid macrophages.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. In this study, we performed scRNA-Seq experiments to gain insights into the transcriptional regulation of polyploid macrophage differentiation in response to chronically persistent inflammatory stimuli. Overall design: scRNA-Seq was performed on FACS-sorted 2c and >4c DNA content polyploid macrophages after six days of bacterial lipoprotein, FSL-1 treatment of bone marrow-derived macrophage precursors. 2c DNA content macrophages treated with M-CSF alone were used as controls. CEL-Seq2 protocol was used for single cell sequencing (Hashimshony et al. 2016).

Publication Title

DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE51014
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways
  • organism-icon Mus musculus, Danio rerio
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE51012
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

The mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart.

Publication Title

Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon SRP030036
Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways
  • organism-icon Danio rerio
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerII

Description

The mammalian heart has poor regenerative capacity following injury. In contrast, certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA-dependant regulatory circuits in the heart. We identified novel miRNA-dependant networks involved in critical biological pathways, which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions, 4 biological replicates per condition

Publication Title

Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA-dependent repair pathways.

Sample Metadata Fields

No sample metadata fields

View Samples
...

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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Developed by the Childhood Cancer Data Lab

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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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