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accession-icon GSE21063
NFATc1 controls the survival, function and suppressive capacity of B lymphocytes upon B cell receptor stimulation
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon

Description

Triggering of B cell receptors (BCR) induces a massive synthesis of NFATc1 in splenic B cells. By inactivating the Nfatc1 gene and re-expressing NFATc1 we show that NFATc1 levels are critical for the survival of splenic B cells upon BCR stimulation. NFATc1 ablation led to decreased BCR-induced Ca++ flux and proliferation of splenic B cells, increased apoptosis and suppressed germinal centre formation and immunoglobulin class switch by T cell-independent antigens. By controlling IL-10 synthesis in B cells, NFATc1 supported the proliferation and IL-2 synthesis of T cells in vitro and appeared to contribute to the mild clinical course of Experimental Autoimmune Encephalomyelitis in mice bearing NFATc1-/- B cells. These data indicate NFATc1 as a key factor controlling B cell function.

Publication Title

NFATc1 affects mouse splenic B cell function by controlling the calcineurin--NFAT signaling network.

Sample Metadata Fields

Specimen part

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accession-icon GSE51686
Fracture healing in osteoporotic mice
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

Genome-wide comparative gene expression analysis of callus tissue of osteoporotic mice (Col1a1-Krm2 and Lrp5-/-) and wild-type were performed to identify candidate genes that might be responsible for the impaired fracture healing observed in Col1a1-Krm2 and Lrp5-/- mice.

Publication Title

Osteoblast-specific Krm2 overexpression and Lrp5 deficiency have different effects on fracture healing in mice.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE57810
Expression profiling of tumor cells from MYCN-driven neuroblastoma upon BRD4 or AURKA inhibition
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Amplification of MYCN is the most prominent genetic marker of high-stage neuroblastoma, a childhood tumor originating from the neural crest. We generated a cell line (mNB-A1) from tumors developed in transgenic mouse and treated these cells with DMSO (n=6), the BRD4-inhibitor JQ1 (n=3) or the AURKA-inhibitor MLN8237 (n=3) for 24 h.

Publication Title

A Cre-conditional MYCN-driven neuroblastoma mouse model as an improved tool for preclinical studies.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE36416
Protein kinase C-beta dependent activation of NF-kB in stromal cells is indispensable for the survival of chronic lymphocytic leukemia in B-cells in vivo.
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Protein kinase c-β-dependent activation of NF-κB in stromal cells is indispensable for the survival of chronic lymphocytic leukemia B cells in vivo.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE36415
Effect of NF-kappaB activation in bone marrow stromal cells co-cultured with CLL cells
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon

Description

Tumor cell survival critically depends on heterotypic communication with benign cells in the microenvironment. Here we describe a novel survival signaling pathway activated in stromal cells by contact to B-cells from chronic lymphocytic leukemia (CLL) patients. The expression of PKC-II and the subsequent activation of NF-B in bone marrow stromal cells is a prerequisite to support the survival of malignant B-cells. PKC- knockout mice are insusceptible to CLL-transplantations, underscoring the in vivo significance of the PKC-II- NF-B signaling pathway in the tumor microenvironment. Upregulated stromal PKC-II in biopsies from CLL, breast- and pancreatic- cancer patients suggest that this pathway may commonly be activated in a variety of malignancies.

Publication Title

Protein kinase c-β-dependent activation of NF-κB in stromal cells is indispensable for the survival of chronic lymphocytic leukemia B cells in vivo.

Sample Metadata Fields

Specimen part

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accession-icon GSE36414
Gene expression changes induced in the stromal cell line EL08-1D2 by co-culture with leukemic B cells (CLL)
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon

Description

Tumor cell survival critically depends on heterotypic communication with benign cells in the microenvironment. Here we describe a novel survival signaling pathway activated in stromal cells by contact to B-cells from chronic lymphocytic leukemia (CLL) patients. The expression of PKC-II and the subsequent activation of NF-B in bone marrow stromal cells is a prerequisite to support the survival of malignant B-cells. PKC- knockout mice are insusceptible to CLL-transplantations, underscoring the in vivo significance of the PKC-II- NF-B signaling pathway in the tumor microenvironment. Upregulated stromal PKC-II in biopsies from CLL, breast- and pancreatic- cancer patients suggest that this pathway may commonly be activated in a variety of malignancies.

Publication Title

Protein kinase c-β-dependent activation of NF-κB in stromal cells is indispensable for the survival of chronic lymphocytic leukemia B cells in vivo.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE44260
Murine germinal center and naive B cells
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon

Description

Gene expressions of murine germinal center and naive B cells on Affymetrix platform

Publication Title

Multiple transcription factor binding sites predict AID targeting in non-Ig genes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE26355
Expression data from early and late born Atoh1 lineages within the E14.5 rhombomere 1 and isthmus
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon

Description

Following neural tube closure at around E9.5, the rhombic lip within the rhombomere 1/isthmus region ("upper rhombic lip") produces a sequence of neuronal lineages that populate the brainstem and cerebellum. The transcription factor Atoh1 (Math1) is required for this specialized neurogenesis, although the genetic programs that delineate the temporal cell fate changes downstream of Atoh1 are not well characterized. We examined the gene expresion changes that take place within Atoh1 lineages

Publication Title

Genes expressed in Atoh1 neuronal lineages arising from the r1/isthmus rhombic lip.

Sample Metadata Fields

Specimen part

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accession-icon GSE43381
Expression profiling across mouse epithelial tissues
  • organism-icon Mus musculus
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon

Description

To characterize genes, pathways, and transcriptional regulators enriched in the mouse cornea, we compared the expression profiles of whole mouse cornea, bladder, esophagus, lung, proximal small intestine, skin, stomach, and trachea.

Publication Title

The Ets transcription factor EHF as a regulator of cornea epithelial cell identity.

Sample Metadata Fields

Specimen part

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accession-icon GSE38123
Expression Profiles of PMH treated with 7M of the genotoxic compound cisplatin
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

The transcriptomic changes induced in primary mouse hepatocytes (C57BL/6 ) by 7M of cisplatin after treatment for 24 and 48h

Publication Title

Characterisation of cisplatin-induced transcriptomics responses in primary mouse hepatocytes, HepG2 cells and mouse embryonic stem cells shows conservation of regulating transcription factor networks.

Sample Metadata Fields

Cell line, Treatment, 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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