Mammary alveologenesis is abrogated in the absence of the transcription factors STAT5A/5B that mediate cytokine signaling. To reveal the underlying causes for this developmental block we studied mammary stem and progenitor cells. While loss of STAT5A/5B did not affect the stem cell population and their ability to form mammary ducts, luminal progenitors were greatly reduced and unable to form alveoli during pregnancy. Temporally-controlled expression of transgenic STAT5A in mammary epithelium lacking STAT5A/5B restored the luminal progenitor population and rescued alveologenesis in a reversible fashion in vivo. Taken together, STAT5A is necessary and sufficient for the establishment of luminal progenitor cells.
Development of mammary luminal progenitor cells is controlled by the transcription factor STAT5A.
Specimen part
View SamplesMndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth and may modify plasmacytoma susceptibility.
Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth, and may modify plasmacytoma susceptibility.
Specimen part, Time
View SamplesThe etiology of autoimmune hepatitis is poorly understood but likely involves Th1 cells producing IFN-. BALB/c background TGF-1-/- mice rapidly develop fulminant Th1-mediated autoimmune hepatitis. Our aims are to profile liver gene expression in TGF-1-/- mice, to identify gene expression pathways dependent on IFN- as possible targets for rational therapy, and to test potential targets directly in vivo in mice.
The role of Ifng in alterations in liver gene expression in a mouse model of fulminant autoimmune hepatitis.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A mouse model of the most aggressive subgroup of human medulloblastoma.
Specimen part
View SamplesMouse models of medulloblastoma are compared to human subgroups through microarray expression and other measures
A mouse model of the most aggressive subgroup of human medulloblastoma.
No sample metadata fields
View SamplesBMPR2 mutation causes pulmonary arterial hypertension (PAH); ACE2 treatment can resolve established BMPR2-mediated PAH. The purpose of this study was to uncover the molecular mechanism behind this.
Cytoskeletal defects in Bmpr2-associated pulmonary arterial hypertension.
Sex, Specimen part, Treatment
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 SamplesThis SuperSeries is composed of the SubSeries listed below.
MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma.
Treatment, Time
View SamplesAll highly and poorly permeable metastases from the same mouse brain were collected by laser capture microdissection. Total RNA from both metastatic lesions and immediate microenvironment was isolated from 5 mice bearing 231-BR metastases. As control 4 healthy mouse brains were included.
Reactive astrocytic S1P3 signaling modulates the blood-tumor barrier in brain metastases.
Subject
View SamplesC2C12 mouse myoblasts expressing RAS mutants identified in human tumors fail to differentiate in low serum media.
MEK inhibition induces MYOG and remodels super-enhancers in RAS-driven rhabdomyosarcoma.
No sample metadata fields
View Samples