Conditional deletion of Geminin from the entire hematopoietic compartment using Vav1:iCre mice led to defective hematopoiesis/dyserythropoiesis in E15.5 mouse embryos.
Geminin deletion increases the number of fetal hematopoietic stem cells by affecting the expression of key transcription factors.
Specimen part
View SamplesWe compared different mouse cancer cell lines to identify their unique cell signatures.
Myeloid-derived interleukin-1β drives oncogenic KRAS-NF-κΒ addiction in malignant pleural effusion.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Mast cells mediate malignant pleural effusion formation.
Specimen part, Cell line
View SamplesNave mast cells were cultured from murine bone marrow using incubation with IL-3 alone (samples 1-4) or IL-3 and KITL (samples 5-8).
Mast cells mediate malignant pleural effusion formation.
No sample metadata fields
View SamplesCytochrome oxydases and quinol monooxygenase were removed from the E. coli genome resulting in oxygen-independent physiology
Deletion of genes encoding cytochrome oxidases and quinol monooxygenase blocks the aerobic-anaerobic shift in Escherichia coli K-12 MG1655.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Alteration of mRNA and microRNA expression profiles in rat muscular type vasculature in early postnatal development.
Sex
View SamplesThis study tested the hypothesis that mRNA expression profiles change in the muscular type rat saphenous artery during early postnatal development. To explore this, we performed mRNA microarray analysis on muscular type saphenous arteries of young (10-12 days) and adult (2-3 months) rats.
Alteration of mRNA and microRNA expression profiles in rat muscular type vasculature in early postnatal development.
Sex
View SamplesThis SuperSeries is composed of the SubSeries listed below.
STAT3 suppresses transcription of proapoptotic genes in cancer cells with the involvement of its N-terminal domain.
Cell line
View SamplesActivation of Signal Transducer and Activator of Transcription 3 (STAT3) is common in prostate cancers. STAT3 may induce cell proliferation and resistance to apoptosis, as well as promote tumor angiogenesis, invasion, and migration by activating gene expression. Many STAT3-dependent transcriptional responses are mediated through protein-protein interactions that involve the amino-terminal domain (N-domain).
STAT3 suppresses transcription of proapoptotic genes in cancer cells with the involvement of its N-terminal domain.
Cell line
View SamplesActivation of Signal Transducer and Activator of Transcription 3 (STAT3) is common in prostate cancers. STAT3 may induce cell proliferation and resistance to apoptosis, as well as promote tumor angiogenesis, invasion, and migration by activating gene expression. Many STAT3-dependent transcriptional responses are mediated through protein-protein interactions that involve the amino-terminal domain (N-domain).
STAT3 suppresses transcription of proapoptotic genes in cancer cells with the involvement of its N-terminal domain.
Cell line
View Samples