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accession-icon GSE38461
Expression data from clone sorted tumor endothelial subsets
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Competitive interactions between emerging blood vessels determine the clonogenic contribution to developing vascualture. Using a multi-color cre reporter, CD31+CD45-VeCad+ clones were isolated and analyzed for expression differences.

Publication Title

Dynamic Patterns of Clonal Evolution in Tumor Vasculature Underlie Alterations in Lymphocyte-Endothelial Recognition to Foster Tumor Immune Escape.

Alternate Accession IDs

E-GEOD-38461

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP049059
c-Myc Transcriptionally Amplifies Sox2 Target Genes to Regulate Self-Renewal in Multipotent Otic Progenitor Cells [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

An immortalized multipotent otic progenitor (iMOP) cell was generated by transient expression of c-Myc in Sox2-expressing otic progenitor cells. The procedure activated endogenous c-Myc expression in the cells and amplified existing Sox2-dependent transcripts to promote self-renewal. Downregulation of c-Myc expression following growth factor withdrawal resulted in a molecular switch from self-renewal to otic differentiation. Overall design: Progenitor cells from embryonic inner ear that form otospheres were infected with a c-Myc retrovirus to promote self-renewal

Publication Title

SHIELD: an integrative gene expression database for inner ear research.

Alternate Accession IDs

GSE62512

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP157976
Acetyl-CoA carboxylase inhibition regulates microtubule dynamics and intracellular transport in cystic fibrosis epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

In this study, we hypothesize that acetyl CoA carboxylase (ACC) is an important intermediate in Cystic fibrosis (CF) inflammatory signaling cascade. Here, we demonstrate that ACC inhibition mimics the cellular effects of ibuprofen promoting both redistribution of intracellular cholesterol and increased rates of microtubule reformation, while decreasing RhoA expression in CF epithelial cell models. Inhibiting ACC polymerization with citrate increases RhoA expression and decreases microtubule reformation rates in wild-type epithelial cells, suggesting pro-inflammatory signaling. Together, these findings demonstrate a novel mechanism of high-dose ibuprofen efficacy and point to a potential new therapeutic target for anti-inflammatory drugs in CF. Overall design: Compare broader impact of ACC inhibition on TOFA-treated (5-(Tetradecyloxy-2-furoic acid) CF HNE cells

Publication Title

Acetyl-CoA carboxylase inhibition regulates microtubule dynamics and intracellular transport in cystic fibrosis epithelial cells.

Alternate Accession IDs

GSE118567

Sample Metadata Fields

Sex, Age, Specimen part, Disease, Subject

View Samples
accession-icon SRP045182
Gene Expression by Mouse Inner Ear Hair Cells During Development
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Hair cells of the inner ear are essential for hearing and balance. As a consequence, pathogenic variants in genes specifically expressed in hair cells often cause hereditary deafness. Hair cells are few in number and not easily isolated from the adjacent supporting cells, so the biochemistry and molecular biology of hair cells can be difficult to study. To study gene expression in hair cells, we developed a protocol for hair cell isolation by FACS sorting. With nearly pure hair cells and surrounding cells, from cochlea and utricle and from embryonic day 16 to postnatal day 7, we performed a comprehensive cell-type-specific RNA-Seq study of gene expression during mouse inner ear development. Expression profiling revealed new hair-cell genes with distinct expression patterns: some are specific for vestibular hair cells, others for cochlear hair cells, and some are expressed just before or after maturation of mechanosensitivity. We found that many of the known hereditary deafness genes are much more highly expressed in hair cells than surrounding cells, suggesting that genes preferentially expressed in hair cells are good candidates for unknown deafness genes. Overall design: 3' tags of mRNA profiles of hair cells and surrounding cells from E16, P0, P4, and P7 cochlear and utricular sensory epithelia were generated by deep sequencing, using Illumina GAIIx

Publication Title

XIRP2, an actin-binding protein essential for inner ear hair-cell stereocilia.

Alternate Accession IDs

GSE60019

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE27982
Genetic and pharmacologic approach to identify genes regulated by mTORC1
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a critical regulator of cell growth by integrating multiple signals (nutrients, growth factors, energy and stress) and is frequently deregulated in many types of cancer. We used a robust experimental paradigm involving the combination of two interventions, one genetic and one pharmacologic to identify genes regulated transcriptionally by mTORC1. In Tsc2+/+, but not Tsc2-/- immortalized mouse embryo fibroblasts (MEFs), serum deprivation downregulates mTORC1 activity. In Tsc2-/- cells, abnormal mTORC1 activity can be downregulated by treatment with rapamycin (sirolimus). By contrast, rapamycin has little effect on mTORC1 in Tsc2+/+ cells in which mTORC1 is already inhibited by low serum. Thus, under serum deprived conditions, mTORC1 activity is low in Tsc2+/+ cells (untreated or rapamycin treated), high in Tsc2-/- cells, but lowered by rapamycin; a pattern referred to as a low/low/high/low or LLHL, which allowed the identification of genes regulated by mTORC1 by performing the appropriate comparisons

Publication Title

Regulation of TFEB and V-ATPases by mTORC1.

Alternate Accession IDs

E-GEOD-27982

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP108222
AR-independent prostate cancer is sustained through FGF signaling
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Androgen receptor (AR) signaling is a distinctive feature of prostate cancer (PC) and represents the major therapeutic target for the treatment of metastatic disease. Though highly effective, AR antagonism has the potential to generate tumors that bypass a functional requirement for AR activity. We show here that a phenotypic shift has occurred in metastatic PCs with the emer-gence of a double-negative AR-null neuroendocrine-null phenotype that is notable for MAPK and FGF pathway activity. To identify mechanisms capable of sustaining PC survival, we gener-ated a model system designated AR program-independent prostate cancer (APIPC) which re-sists AR-targeted therapeutics, lacks neuroendocrine features, expresses high levels of FGF8 and the ID1 oncogene, and activates MAPK signaling. Pharmacological blockade of MAPK or FGF signaling inhibited APIPC tumor growth, supporting FGF/MAPK as a therapeutic avenue for treating AR-null PC. Overall design: RNA sequencing of human prostate tumor cell lines using the Illumina TruSeq Library prep and sequenced on Illumina HiSeq 2500.

Publication Title

Androgen Receptor Pathway-Independent Prostate Cancer Is Sustained through FGF Signaling.

Alternate Accession IDs

GSE99381

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

View Samples
accession-icon GSE37563
In vivo gene expression data from wild type and CTLA-4 KO 5C.C7 T cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

CTLA-4 is thought to inhibit effector T cells both intrinsically, by competing with CD28 for B7 ligands, and extrinsically, through the action of regulatory T cells. We studied in vivo responses of normal and CTLA-4-deficient antigen-specific murine effector CD4+ T cells. In order to do these studies in a physiological model of immunity to foreign antigen, we transferred small numbers of congenically marked RAG2-deficient 5C.C7 T cells with either a normal or knockout allele of CTLA-4 into normal syngeneic B10.A recipient mice. The T cells were then activated by immunization with MCC peptide and LPS. To look for transcriptional signatures of negative regulation of T cell responses by CTLA-4, we used microarray analysis to compare transcripts in wild type and CTLA-4 KO 5C.C7 T cells four days after immunization. This is the first instance in which differences are observed in extent of accumulation of wild type and CTLA-4 KO 5C.C7 T cells.

Publication Title

Cutting edge: CTLA-4 on effector T cells inhibits in trans.

Alternate Accession IDs

E-GEOD-37563

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP084270
Inhibition of ERG Activity in Patient Derived Prostate Cancer Xenografts using the Small Molecule Inhibitor YK-4-279
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

ERG activity was blocked using YK-4-279 in three subcutaneously implanted ERG+ (LuCaP 23.1, 86.2, and 35) and one ERG- (LuCaP 96) PDX. Tumor volume (TV), body weight (BW), serum prostate specific antigen (PSA), and overall survival (OS) were compared to vehicle treated controls. Changes in gene expression were assessed by RNASeq and tissue microarrays were constructed to assess necrosis, proliferation, apoptosis, microvessel density, and ERG expression. Overall design: RNA sequencing of tumors from from 16 animals (2 control, 2 treated from each of four patient derived xenograft lines) using Illumina HiSeq 2500.

Publication Title

Inhibition of ERG Activity in Patient-derived Prostate Cancer Xenografts by YK-4-279.

Alternate Accession IDs

GSE86387

Sample Metadata Fields

Sex, Treatment, Subject

View Samples
accession-icon SRP200599
Identification of genes with enriched expression in early developing mouse cone photoreceptors
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

A LHX4 transgenic reporter line with high specificity for developing mouse cone photoreceptors was identified and used to purify early stage cone photoreceptors for profiling by single cell RNA sequencing. Overall design: Collection of FACS-sorted LHX4::GFP+ E14.5 early cones and LHX4::GFP- retinal cells for further analysis.

Publication Title

Identification of Genes With Enriched Expression in Early Developing Mouse Cone Photoreceptors.

Alternate Accession IDs

GSE132272

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon GSE85672
Characterization of an abiraterone ultra-responsive phenotype in castration-resistant prostate cancer patient-derived xenografts
  • organism-icon Homo sapiens
  • sample-icon 69 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

To identify the molecular signature associated with abiraterone acetate (AA) response and mechanisms underlying AA resistance in castration-resistant prostate cancer patient-derived xenografts (PDXs).

Publication Title

Characterization of an Abiraterone Ultraresponsive Phenotype in Castration-Resistant Prostate Cancer Patient-Derived Xenografts.

Alternate Accession IDs

E-GEOD-85672

Sample Metadata Fields

Specimen part, Treatment

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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