The spinal cords of mice submitted to aortic cross-clamping for 7.5 minutes present with gray matter damage and central cord edema. 60% of mice subsequently experience hindlimb and tail paralysis.
No associated publication
Specimen part
View SamplesTo 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.
E2f1-3 are critical for myeloid development.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Canonical and atypical E2Fs regulate the mammalian endocycle.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.
Specimen part
View SamplesTo 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.
Canonical and atypical E2Fs regulate the mammalian endocycle.
Age, Specimen part
View SamplesLoss of Myc corrects abrrant transcription in Rb KO villi, while these genetic manipulation does not lead to major gene expression changes in crypts.
No associated publication
Specimen part
View SamplesRb and E2F are thought to play antagonistic roles in celll proliferation. However, this model is based mostly from in vitro cell culture systems. We used small intestines to test this model in vivo.
E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells.
Age, Specimen part
View SamplesPTEN imparts tumor suppression in mice by cell autonomous and non-autonomous mechanisms. Whether these two tumor suppressor roles are mediated through similar or distinct signaling pathways is not known. Here we generated and analyzed knockin mice that express a series of human cancer-derived mutant alleles of PTEN in either stromal or tumor cell compartments of mammary glands. We find that cell non-autonomous tumor suppression by Pten in stromal fibroblasts strictly requires activation of P-Akt signaling, whereas cell autonomous tumor suppression in epithelial tumor cells is independent of overt canonical pathway activation
Noncatalytic PTEN missense mutation predisposes to organ-selective cancer development in vivo.
Age, Specimen part
View SamplesmiR-155 transgenic mice develop pre-B cell leukemia/lymphoma. Though some targets of miR-155 are known, understanding of the mechanism by which miR-155 overexpression drives malignant transformation is not known. MicroRNAs regulate multiple genes.
miR-155 targets histone deacetylase 4 (HDAC4) and impairs transcriptional activity of B-cell lymphoma 6 (BCL6) in the Eμ-miR-155 transgenic mouse model.
No sample metadata fields
View SamplesThe function of ID4 in CLL development was studied in vivo using TCL1 transgenic mouse model that develop leukemia similar to human CLL. TCL1 mice with ID4 single knockout gene have accelerated CLL progression.
Silencing of the inhibitor of DNA binding protein 4 (ID4) contributes to the pathogenesis of mouse and human CLL.
Specimen part
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