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accession-icon GSE27038
Expression data from the Ire1 null and control murine livers in the absence or presence of ER stress
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
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Description

Ire1 conditional null or control mice of 3-months old were injected intraperitoneally with TM or vehicle.

Publication Title

The unfolded protein response transducer IRE1α prevents ER stress-induced hepatic steatosis.

Sample Metadata Fields

Specimen part

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accession-icon GSE16522
Effector cells derived from nave or central memory pmel-1 CD8+ T cells
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
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Description

Effector cells for adoptive immunotherapy can be generated by in vitro stimulation of nave or memory subsets of CD8+ T cells. While the characteristics of CD8+ T cell subsets are well defined, the heritable influence of those populations on their effector cell progeny is not well understood. We studied effector cells generated from nave or central memory CD8+ T cells and found that they retained distinct gene expression signatures and developmental programs. Effector cells derived from central memory cells tended to retain their CD62L+ phenotype, but also to acquire KLRG1, an indicator of cellular senescence. In contrast, the effector cell progeny of nave cells displayed reduced terminal differentiation, and, following infusion, they displayed greater expansion, cytokine production, and tumor destruction. These data indicate that effector cells retain a gene expression imprint conferred by their nave or central memory progenitors, and they suggest a strategy for enhancing cancer immunotherapy.

Publication Title

Adoptively transferred effector cells derived from naive rather than central memory CD8+ T cells mediate superior antitumor immunity.

Sample Metadata Fields

Specimen part

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accession-icon GSE32355
E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells
  • organism-icon Mus musculus
  • sample-icon 101 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Canonical and atypical E2Fs regulate the mammalian endocycle.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE32354
Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix)
  • organism-icon Mus musculus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon

Description

To understand the underlying cause and mechanisms of changes in hepatocyte ploidy upon Albumin-Cre mediated deletion of E2f7&8 and Mx1-Cre mediated deletion of E2f1,2&3, we analysed global gene expression of 6 weeks and 2 months liver tissues.

Publication Title

Canonical and atypical E2Fs regulate the mammalian endocycle.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE25825
Expression data from MxCre;E2F1-/-2-/-3f/f Cd11B myeloid cells
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
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Description

To understand the underlying cause for the observed apoptosis in E2f1-3 deficient myeloid cells. We compared gene expression profiles of Cd11b+ sorted myeloid cells isolated from bone marrow of control (E2F1-/- ) and experimental (Mxcre;E2F1-/-2-/-3f/f ) mice.

Publication Title

E2f1-3 are critical for myeloid development.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE42135
Expression data from preimplantation mouse embryos
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
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Description

Landmark events occur in a coordinated manner during preimplantation development of the mammalian embryo, yet the regulatory network that orchestrates these events remains largely unknown.

Publication Title

An Oct4-Sall4-Nanog network controls developmental progression in the pre-implantation mouse embryo.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44166
Expression Data from Normal or ErbB2 Tumor Fibroblasts With or Without Ets2
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
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Description

The mechanisms involved in epithelium-stroma interactions remain poorly understood, despite the importance of the microenvironment during tumorigenesis. Here, we studied the role of Ets2 transcrpiton factor in tumor associated fibroblasts in the MMTV-ErbB2 mammary tumor model. Inactivation of Ets2 specifically in fibroblasts using Fsp-cre significantly reduced tumor growth, in contrast to Ets2 inactivation in epithelium in which no differences in tumor growth were observed.

Publication Title

Ets2 in tumor fibroblasts promotes angiogenesis in breast cancer.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE13245
Hepatic gene expression during the development of experimental biliary atresia in different mouse strains
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
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Description

Biliary atresia (BA) is a rare cholestatic disease of unknown etiology that affects infants and shows an incidence of 1 out of 18,000 live births in Europe (1). The first therapeutic option is a timely performed portoenterostomy. However, the majority of patients suffer from a progressive inflammatory process, which leads to complete destruction of the extra- and intrahepatic biliary system followed by end-stage liver cirrhosis. Hence, BA is the leading indication for pediatric liver transplantation worldwide (2, 3). To understand the pathogenesis of the disease and improve theoutcome of BA patients, research has focused on the inflammatory process in liver and bile ducts, in which several factors are remarkably elevated, such as activated CD4 and CD8 T-cells, TNF alpha,IFN alpha and other proinflammatory TH1 cytokines (3-8). By the time of diagnosis, however, the disease has already reached an advanced state, characterized by the complete obstruction of the extrahepatic bile ducts with impaired bile flow and fibrosis or cirrhosis of the liver. Therefore, studies in humans focusing on the trigger mechanism of BA are limited due to the paucity of liver and availability of bile duct tissue for research. One infectious animal model has been developed, in which newborn Balb/c mice exclusively show the experimental BA phenotype after infection with rhesus rotavirus (RRV) (9, 10). This model allows the analysis of the inflammatory reactions in liver and bile ducts at early steps in the development of bile duct atresia (11-20). Furthermore, inbred mouse strains have been shown to have a different susceptibility for the development of experimental BA, suggesting that Balb/c mice have an immunological gap responsible for disease progression (10, 12). The aim of this study was to identify key genes responsible for the BA phenotype by comparing the transcriptomes at an early time point after virus infection, i.e. before bile duct atresia, between two mouse strains with different susceptibilities to BA. Differences in the virus titration and the clinical course of infected mice were analyzed, and variations in the hepatic gene response assessed by comparative microarray assays were correlated to variances in the hepatic inflammatory reaction.

Publication Title

Susceptibility to experimental biliary atresia linked to different hepatic gene expression profiles in two mouse strains.

Sample Metadata Fields

Specimen part

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accession-icon GSE56009
E2f and Myc transcriptional programs and chromatin binding landscapes in the small intestines
  • organism-icon Mus musculus
  • sample-icon 30 Downloadable Samples
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Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.

Sample Metadata Fields

Specimen part

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accession-icon GSE53590
Dietary fat disturbance of of gut microbial diurnal patterns uncouples host metabolic networks.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Diet-induced obesity (DIO) is rapidly becoming a global health problem, particularly as Westernization of emerging nations continues. Currently, one third of adult Americans are considered obese and, if current trends continue, >90% of US citizens are predicted to be affected by 2050. However, efforts to fight this epidemic have not yet produced sound solutions for prevention or treatment. Our studies reveal a balanced and chronobiological relationship between food consumption, daily variation in gut microbial evenness and function, basomedial hypothalamic circadian clock (CC) gene expression, and key hepatic metabolic regulatory networks , including CC and nuclear receptors (NR), that is are essential for metabolic homeostasis. Western diets high in saturated fats dramatically alter diurnal variation in microbial composition and function, which in turn lead to uncoupling of the hepatic CC and NR networks from central CC control in ways that offset the timing and types of regulatory factors directing metabolic function. These signals include microbial metabolites such as short chain fatty acids (SCFAs) and hydrogen sulfide (H2S) that can directly regulate or disrupt metabolic networks of the hepatocyte. Our study therefore provides insights into the complex and dynamic relationships between diet, gut microbes, and the host that are critical for maintenance of health. Perturbations of this constellation of processes, in this case by diet-induced dysbiosis and its metabolomic signaling, can potentially promote metabolic imbalances and disease. This knowledge opens up many possibilities for novel therapeutic and interventional strategies to treat and prevent DIO, ranging from the manipulation of gut microbial function to pharmacological targeting of host pathways to restore metabolic balance.

Publication Title

Effects of diurnal variation of gut microbes and high-fat feeding on host circadian clock function and metabolism.

Sample Metadata Fields

Specimen part

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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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