This SuperSeries is composed of the SubSeries listed below.
The impact of microRNAs on protein output.
No sample metadata fields
View SamplesThis array analysis is to study the regulation of target messages expression in in vitro cultured murine neutrophils versus miR-223 null neutrophils. Culture media was SILAC-IMDM for MS analysis.
The impact of microRNAs on protein output.
No sample metadata fields
View SamplesThis array analysis is to study the regulation of target messages expression in murine neutrophils versus miR-223 null neutrophils.
The impact of microRNAs on protein output.
No sample metadata fields
View SamplesThese arrays contain data from hypthalamus tissue of nestin-Pex5 -/- male mice
Peroxisome deficiency but not the defect in ether lipid synthesis causes activation of the innate immune system and axonal loss in the central nervous system.
Specimen part
View SamplesTo study the possible fibrotic role of FIZZ2, bleomycin was used to induce pulmonary fibrosis in wild type and FIZZZ2 knockout mice, lungs were then harvested and processed for RNA isolation.
FIZZ2/RELM-β induction and role in pulmonary fibrosis.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
An integrated systems biology approach identifies positive cofactor 4 as a factor that increases reprogramming efficiency.
Sex, Specimen part
View SamplesMultipotent spermatogonial stem cells (mSSCs) derived from SSCs are a potential new source of individualized pluripotent cells in regenerate medicine such as ESCs. We hypothesized that the culture-induced reprogramming of SSCs was mediated by a mechanism different from that of iPS, and was due to up-regulation of specific pluripotency-related genes during cultivation. Through a comparative analysis of expression profile data, we try to find cell reprogramming candidate factors from mouse spermatogonial stem cells. We used microarrays to analyze the gene expression profiles of culture-induced reprogramming converting unipotent spermatogonial stem cells to pluripotent spermatogonial stem cells.
An integrated systems biology approach identifies positive cofactor 4 as a factor that increases reprogramming efficiency.
Sex, Specimen part
View SamplesCells located at the invasive front and in the tumor mass of mouse cervical squamous cell carcinomas were isolated by laser microdissection from hematoxylin-stained HPV/E2 sections. 7 months old HPV/E2 mice treated with oestrogen develop invasive cervical squamous cell carcinomas. This model recapitulates human invasive cervical neoplasias.
Inflammatory Cytokines Induce Podoplanin Expression at the Tumor Invasive Front.
Specimen part
View SamplesBackground
Similar inflammatory DC maturation signatures induced by TNF or Trypanosoma brucei antigens instruct default Th2-cell responses.
Specimen part, Treatment
View SamplesSTAT5 is critical for differentiation, proliferation and survival of progenitor B cells suggesting a possible role in Acute Lymphoblastic Leukemia (ALL). Herein, we show increased expression of activated STAT5 in ALL patients, which correlates with treatment outcome. Mutations in Ebf1 and Pax5, genes critical for B cell development have also been identified in human ALL. To determine whether mutations in Ebf1 or Pax5 synergize with STAT5 activation to induce ALL we crossed mice expressing a constitutively active form of STAT5 (Stat5b-CA) with mice heterozygous for Ebf1 or Pax5. Haploinsufficiency of either Pax5 or Ebf1 synergized with Stat5b-CA to rapidly induce ALL in 100% of the mice. The leukemic cells displayed reduced expression of both Pax5 and Ebf1 but this had little affect on most EBF1 or PAX5 target genes. However, a subset of these genes was deregulated and included a large percentage of potential tumor suppressor genes and oncogenes. Further, most of these genes appear to be jointly regulated by both EBF1 and PAX5. Our findings suggest a model whereby small perturbations in a self-reinforcing network of transcription factors critical for B cell development, specifically PAX5 and EBF1, cooperate with STAT5 activation to initiate ALL.
Ebf1 or Pax5 haploinsufficiency synergizes with STAT5 activation to initiate acute lymphoblastic leukemia.
No sample metadata fields
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