Prophase I of meiosis involves dynamic chromosome segregation processes including synapsis, meiotic recombination, and cohesion. Genetic defects in genes participating in these processes consistently cause reproduction failure in mice. To identify candidate genes responsible for infertility or recurrent pregnancy loss in humans, we performed expression profiling of male and female gonads of mice undergoing meiotic prophase I.
Screening of genes involved in chromosome segregation during meiosis I: in vitro gene transfer to mouse fetal oocytes.
Sex, Age, Specimen part
View SamplesThe aim of this study was to examine the role of indigenous lactobacilli in the physiological development of the stomach in mice using microarray analysis. In lactobacilli-associated gnotobiotic mice, an increased expression of the genes related to the muscle system development, such as nebulin and troponin, was observed. On the other hand, the expression of the gastrin gene dramatically decreased. A microarray analysis of the stomachs infected with H. pylori also showed both the up-regulation of muscle cell genes and the down-regulation of gastrin genes.
Role of indigenous lactobacilli in gastrin-mediated acid production in the mouse stomach.
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View Samplesgenes regualted by LPS or LPS+cAMP stimulation in BMDCs
Cyclic adenosine monophosphate suppresses the transcription of proinflammatory cytokines via the phosphorylated c-Fos protein.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
An integrated approach to dissecting oncogene addiction implicates a Myb-coordinated self-renewal program as essential for leukemia maintenance.
Specimen part, Treatment
View SamplesTo explore oncogene addiction programs in a genetically defined leukemia context we developed an AML mouse model driven by a conditional MLL-AF9 allele together with oncogenic Ras, which enabled us to examine the consequences of MLL-AF9 inhibition in established disease. In order to produce a tightly regulated system that was easy to monitor, we constructed two retroviral vectors containing dsRed-linked MLL-AF9 under control of a tetracycline response element promoter, and KrasG12D or NrasG12D linked to the Tet-off tet-transactivator, which activates TRE expression in a doxycycline repressible manner. Leukemias were generated by retroviral cotransduction of both vectors into hematopoietic stem and progenitor cells, which were transplanted into syngeneic mice. Cells harboring both constructs induced aggressive myelomonocytic leukemia. Five independent primary leukemia cell lines were established from bone marrow of terminal mice. Treatment of these lines with doxycycline rapidly turned off MLL-AF9 expression, and induced terminal myeloid differentiation and complete disease remission in vivo.
An integrated approach to dissecting oncogene addiction implicates a Myb-coordinated self-renewal program as essential for leukemia maintenance.
Specimen part, Treatment
View SamplesUsing an integrative approach combining a Tet-off conditional AML mouse model, global expression profiling following suppression of the driving MLL-AF9 oncogene, and a new Tet-on conditional shRNA expression system we have identified Myb as critical mediator of addiction to MLL-AF9. Suppression of Myb in established AML in vivo terminates aberrant self-renewal and triggers a terminal myeloid differentiation program that precisely phenocopies the effects of suppressing MLL-AF9. Remarkably, suppressing Myb effectively eradicates aggressive and chemotherapy resistant AML.
An integrated approach to dissecting oncogene addiction implicates a Myb-coordinated self-renewal program as essential for leukemia maintenance.
Specimen part
View Samples