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accession-icon GSE25527
Cleavage of NIK by the API2-MALT1 Fusion Oncoprotein Leads to Noncanonical NF-{kappa}B Activation
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Proper regulation of nuclear factor B (NF-B) transcriptional activity is required for normal lymphocyte function, and deregulated NF-B signaling can facilitate lymphomagenesis. We demonstrate that the API2-MALT1 fusion oncoprotein created by the recurrent t(11;18)(q21;q21) in mucosa-associated lymphoid tissue (MALT) lymphoma induces proteolytic cleavage of NF-Binducing kinase (NIK) at arginine 325. NIK cleavage requires the concerted actions of both fusion partners and generates a C-terminal NIK fragment that retains kinase activity and is resistant to proteasomal degradation. The resulting deregulated NIK activity is associated with constitutive noncanonical NF-B signaling, enhanced B cell adhesion, and apoptosis resistance. Our study reveals the gain-of-function proteolytic activity of a fusion oncoprotein and highlights the importance of the noncanonical NF-B pathway in B lymphoproliferative disease.

Publication Title

Cleavage of NIK by the API2-MALT1 fusion oncoprotein leads to noncanonical NF-kappaB activation.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE25550
t(11;18)-positive vs. t(11;18)-negative MALT lymphoma
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Comparison of t(11;18)-positive MALT lymphoma to t(11;18)-negative MALT lymphoma, with a special focus on the NF-KB pathway and it's targets

Publication Title

Cleavage of NIK by the API2-MALT1 fusion oncoprotein leads to noncanonical NF-kappaB activation.

Sample Metadata Fields

Specimen part

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accession-icon GSE7219
NIK/NF-kappaB2 regulated gene products.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This study aims at identifying genes that are NIK/NF-kappaB2 responsive in murine dendritic cells matured in vivo.

Publication Title

Dendritic cells require the NF-kappaB2 pathway for cross-presentation of soluble antigens.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE52577
PU.1 promotes cell cycle exit in the murine myeloid lineage associated with down-regulation of E2F1
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

A doxycycline-inducible system was used to induce PU.1 expression in cultured myeloid cell lines. The parent cell line used was BN (Kamath et al., Leukemia 22:1214-1225, 2008).

Publication Title

PU.1 promotes cell cycle exit in the murine myeloid lineage associated with downregulation of E2F1.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE69818
COPD lung tissue expression
  • organism-icon Homo sapiens
  • sample-icon 70 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Comparison of emphysema vs non emphysema COPD lung tissue expression

Publication Title

Network Analysis of Lung Transcriptomics Reveals a Distinct B-Cell Signature in Emphysema.

Sample Metadata Fields

Specimen part

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accession-icon GSE21858
Patterns of gene expression and evolution in the human developing cerebral cortex
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The cerebral cortex underwent a rapid expansion and complexification during recent primate evolution, but the underlying developmental mechanisms remain essentially unknown.

Publication Title

Genes expressed in specific areas of the human fetal cerebral cortex display distinct patterns of evolution.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE60356
Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Retinoic acid is essential for Th1 cell lineage stability and prevents transition to a Th17 cell program.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE60354
Retinoic acid signaling constrains the plasticity of Th1 cells and prevents development of pathogenic Th17 cells [Affymetrix experiments]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st), Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray (Probe Name version)

Description

CD4+ T cells differentiate into phenotypically distinct T-helper cells upon antigenic stimulation. Regulation of plasticity between these CD4+ T-cell lineages is critical for immune homeostasis and prevention of autoimmune diseases. However, the factors that regulate lineage stability are largely unknown. Here we investigate a role for retinoic acid (RA) in the regulation of lineage stability using T helper 1 (Th1) cells, traditionally considered the most phenotypically stable Th subset. We found that RA, through its receptor RARa, sustains stable expression of Th1 lineage specifying genes as well as repressing genes that instruct Th17 cell fate. RA signaling is essential for limiting Th1 cell conversion into Th17 effectors and for preventing pathogenic Th17 responses in vivo. Our studies identify RA-RARa as a key component of the regulatory network governing Th1 cell fate and define a new paradigm for the development of pathogenic Th17 cells. These findings have important implications for autoimmune diseases in which dysregulated Th1-Th17 responses are observed.

Publication Title

Retinoic acid is essential for Th1 cell lineage stability and prevents transition to a Th17 cell program.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE33903
Expression array of peripheral neuro-ectodermal cell lines
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To study differentially expressed genes in neuro-ectodermal cell lines

Publication Title

Downregulation of Axl in non-MYCN amplified neuroblastoma cell lines reduces migration.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE9816
Gene expression profiling of sav mutants
  • organism-icon Arabidopsis thaliana
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Plants grown at high densities perceive a decrease in the red to far-red (R:FR) ratio of incoming light, resulting from absorption of red light by canopy leaves and reflection of far-red light from neighboring plants. These changes in light quality trigger a series of responses known collectively as the shade avoidance syndrome. During shade avoidance, stems elongate at the expense of leaf and storage organ expansion, there is reduced branching, and flowering is accelerated. We identified several loci in Arabidopsis, mutations in which lead to plants defective in multiple shade avoidance outputs. Here we describe SAV3, an aminotransferase, and show that SAV3 catalyzes the formation of indole-3-pyruvic acid (IPA) from L-tryptophan (L-Trp), the first step in a previously proposed, but uncharacterized, auxin biosynthetic pathway. This pathway can be rapidly deployed to biosynthesize auxin at the high levels required to initiate the multiple changes in body plan associated with shade avoidance.

Publication Title

Rapid synthesis of auxin via a new tryptophan-dependent pathway is required for shade avoidance in plants.

Sample Metadata Fields

Age, 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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