A comparative analysis of gene expression of CD4+ EGFP+ Nrp1+ (tTreg, thymus-derived Treg), CD4+ EGFP+ Nrp1- (pTreg, peripherally-derived Treg) and CD4+ EGFP- (Tconv, conventional T cell) in CD28-/- Foxp3EGFP and Foxp3EGFP mice. Overall design: Nrp1+ Treg (tTreg), Nrp1- Treg (pTreg) and Tconv were sorted from Foxp3EGFP and CD28-/-Foxp3EGFP mice. Total RNAs were extracted from whole samples and analyzed by RNA-seq.
CD28 co-stimulation is dispensable for the steady state homeostasis of intestinal regulatory T cells.
Specimen part, Cell line, Subject
View SamplesThe oviducts play a critical role in gamete and embryo transport, as well as supporting fertilization and early embryo development. Progesterone receptor (PGR) is a transcription factor highly expressed in oviductal cells, while its activating ligand, progesterone (P4), surges to peak levels as ovulation approaches. P4 is known to regulate oviduct cilia beating and muscular contractions in vitro, but how PGR may mediate this in vivo is poorly understood. We used PGR-knockout (PRKO) mice to determine how PGR regulates oviductal function during the periovulatory period, in particular oviductal transport and embryo support.
Progesterone receptor-dependent regulation of genes in the oviducts of female mice.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Regulation of the ovarian inflammatory response at ovulation by nuclear progesterone receptor.
No sample metadata fields
View SamplesOvulation requires sequential molecular events and structural remodeling in the ovarian follicle for the successful release of a mature oocyte capable of being fertilised. Critical to this process is progesterone receptor (PGR), a transcription factor highly yet transiently expressed in granulosa cells of preovulatory follicles. Progesterone receptor knockout (PRKO) mice are anovulatory, with a specific and complete defect in follicle rupture. Therefore, this model was used to examine the critical molecular and biochemical mechanisms necessary for successful ovulation.
Regulation of the ovarian inflammatory response at ovulation by nuclear progesterone receptor.
No sample metadata fields
View SamplesOvulation requires sequential molecular events and structural remodeling in the ovarian follicle for the successful release of a mature oocyte capable of being fertilised. Critical to this process is progesterone receptor (PGR), a transcription factor highly yet transiently expressed in granulosa cells of preovulatory follicles. Progesterone receptor knockout (PRKO) mice are anovulatory, with a specific and complete defect in follicle rupture. Therefore, this model was used to examine the critical molecular and biochemical mechanisms necessary for successful ovulation.
Regulation of the ovarian inflammatory response at ovulation by nuclear progesterone receptor.
No sample metadata fields
View SamplesAbout 10% of Down syndrome (DS) infants are born with a myeloproliferative disorder (DS-TMD) that spontaneously resolves within the first few months of life. About 20-30% of these infants subsequently develop acute megakaryoblastic leukemia (DS-AMKL). In order to understand differences that may exist between fetal and bone marrow megakaryocyte progenitor cell populations we flow sorted megakaryocyte progenitor cells and performed microarray expression analysis.
Developmental differences in IFN signaling affect GATA1s-induced megakaryocyte hyperproliferation.
Specimen part
View SamplesAbout 10% of Down syndrome (DS) infants are born with a myeloproliferative disorder (DS-TMD) that spontaneously resolves within the first few months of life. About 20-30% of these infants subsequently develop acute megakaryoblastic leukemia (DS-AMKL). In order to understand differences that may exist between fetal and bone marrow megakaryocyte progenitor cell populations we flow sorted megakaryocyte progenitor cells and performed microarray expression analysis.
Developmental differences in IFN signaling affect GATA1s-induced megakaryocyte hyperproliferation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A.
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View SamplesDifferences in the amount of fetal hemoglobin (HbF) that persists into adulthood affect the severity of sickle cell disease and the beta-thalassemia syndromes. Genetic association studies have identified sequence variants in the gene BCL11A that influence HbF levels. Here we examine BCL11A as a potential regulator of HbF expression. The high HbF BCL11A genotype is associated with reduced BCL11A expression. Moreover, abundant expression of full-length forms of BCL11A is developmentally restricted to adult erythroid cells. Down-regulation of BCL11A expression in primary adult erythroid cells leads to robust HbF expression. Consistent with a direct role of BCL11A in globin gene regulation, we find that BCL11A occupies several discrete sites in the beta-globin gene cluster. BCL11A emerges as a therapeutic target for reactivation of HbF in beta-hemoglobin disorders.
Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A.
No sample metadata fields
View SamplesDifferences in the amount of fetal hemoglobin (HbF) that persists into adulthood affect the severity of sickle cell disease and the beta-thalassemia syndromes. Genetic association studies have identified sequence variants in the gene BCL11A that influence HbF levels. Here we examine BCL11A as a potential regulator of HbF expression. The high HbF BCL11A genotype is associated with reduced BCL11A expression. Moreover, abundant expression of full-length forms of BCL11A is developmentally restricted to adult erythroid cells. Down-regulation of BCL11A expression in primary adult erythroid cells leads to robust HbF expression. Consistent with a direct role of BCL11A in globin gene regulation, we find that BCL11A occupies several discrete sites in the beta-globin gene cluster. BCL11A emerges as a therapeutic target for reactivation of HbF in beta-hemoglobin disorders.
Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A.
No sample metadata fields
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