The aim of the dataset was to study on genome-wide level the effect of PIM kinase (PIM1+PIM2+PIM3) knockdown in gene expression on early differentiation of human cord blood derived CD4+ T cells cultured under Th1 (Act+IL12) polarizing conditions.
Proviral integration site for Moloney murine leukemia virus (PIM) kinases promote human T helper 1 cell differentiation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Interacting chemokine signals regulate dendritic cells in acute brain injury.
Sex, Specimen part
View SamplesWe inflicted TBI to wildetype (wt) mice in order to establish whether the anti-inflammatory agent cyclophosphamide can be used therapeutically.
Interacting chemokine signals regulate dendritic cells in acute brain injury.
Sex, Specimen part
View SamplesWe inflicted TBI to chemokine-deficient mouse lines in order to establish involvement of various signalling pathways that may be addressed therapeutically.
Interacting chemokine signals regulate dendritic cells in acute brain injury.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The histone methyltransferase SETDB1 represses endogenous and exogenous retroviruses in B lymphocytes.
Specimen part
View SamplesGenome stability relies on epigenetic mechanisms that enforce repression of endogenous retroviruses (ERVs). Current evidence suggests that distinct chromatin-based mechanisms repress ERVs in cells of embryonic origin (histone methylation-dominant) versus more differentiated cells (DNA methylation-dominant). However, the latter aspect of this model has not been tested. Remarkably, and in contrast to the prevailing model, we find that repressive histone methylation catalyzed by the enzyme SETDB1 is critical for suppression of specific ERV families and exogenous retroviruses in committed B-lineage cells from adult mice. The profile of ERV activation in SETDB1-deficient B cells is distinct from that observed in corresponding embryonic tissues, despite the loss of repressive chromatin modifications at all ERVs. We provide evidence that, upon loss of SETDB1, ERVs are activated in a lineage-specific manner depending on the set of transcription factors available to target proviral regulatory elements. These findings have important implications for genome stability in somatic cells, as well as the interface between epigenetic repression and viral latency.
The histone methyltransferase SETDB1 represses endogenous and exogenous retroviruses in B lymphocytes.
Specimen part
View SamplesGenome stability relies on epigenetic mechanisms that enforce repression of endogenous retroviruses (ERVs). Current evidence suggests that distinct chromatin-based mechanisms repress ERVs in cells of embryonic origin (histone methylation-dominant) versus more differentiated cells (DNA methylation-dominant). However, the latter aspect of this model has not been tested. Remarkably, and in contrast to the prevailing model, we find that repressive histone methylation catalyzed by the enzyme SETDB1 is critical for suppression of specific ERV families and exogenous retroviruses in committed B-lineage cells from adult mice. The profile of ERV activation in SETDB1-deficient B cells is distinct from that observed in corresponding embryonic tissues, despite the loss of repressive chromatin modifications at all ERVs. We provide evidence that, upon loss of SETDB1, ERVs are activated in a lineage-specific manner depending on the set of transcription factors available to target proviral regulatory elements. These findings have important implications for genome stability in somatic cells, as well as the interface between epigenetic repression and viral latency. Overall design: Expression profiling and bisulfite PCR sequencing in Setdb1 C/C and Setdb1 D/D pro-B cells
The histone methyltransferase SETDB1 represses endogenous and exogenous retroviruses in B lymphocytes.
No sample metadata fields
View SamplesMultiple myeloma is a fatal hematological malignancy. In order to develop effective therapeutic approaches, it is critical to understand the pathogenesis of myeloma. The Radl 5T model of multiple myeloma is a clinically relevant murine model where myeloma spontaneously occurs in aged, in-bred C57BlKalwRij mice and can be propagated by intravenous inoculation of 5T myeloma cells into mice of the same strain. Importantly inoculation of 5T myeloma cells into C57Bl6 mice does not result in myeloma, demonstrating that the bone marrow (BM) microenvironment of the C57BlKalwRij strain provides a unique and permissive milieu for myeloma development. We hypothesized that cells of the BM microenvironment may provide essential stimuli for the development of multiple myeloma in vivo. We aim to determine the differences in expression within the bone marrow of C57Bl/KalwRij mice.
Host-derived adiponectin is tumor-suppressive and a novel therapeutic target for multiple myeloma and the associated bone disease.
No sample metadata fields
View SamplesNr4a1 deficient rats (Nr4a1-/-) were developed using the fawn hooded hypertensive rat (FHH), which provided a genetic background susceptible to kidney injury. Both groups of animals were evaluated for blood pressure, proteinuria, renal function, and whole transcriptome gene pathway changes. Gene expression profiling was performed at week 8, 16, and 24 using kidney from FHH and Nr4a1-/- rats. To identify differentially expressed gene between FHH and Nr4a1-/- two statistical methods were utilized: (1) FWER (family-wise error rate) procedure, p<0.05 and fold-change 1.2 or greater; and/or (2) Benjamani and Hochberg FDR (false discovery rate) using p<0.05, and fold-change 1.2 or greater. Two-way ANOVA using a p<0.01 or lower was performed to identify strain X time interaction effects between groups. Gene networks and functional analysis were evaluated through the use of Ingenuity Pathways Analysis .
Genetic susceptibility and loss of Nr4a1 enhances macrophage-mediated renal injury in CKD.
Age, Specimen part
View SamplesWe recently developed a new model of renal agenesis [i.e., the heterogeneous stock derived model of unilateral renal agenesis, (HSRA)]. The HSRA model consistently exhibits unilateral renal agenesis ranging from 50-75% in each generation and is characterized by low nephron number, early kidney hypertrophy, and an inherent susceptibility to develop significant kidney injury and decline in renal function with age.
Nephron Deficiency and Predisposition to Renal Injury in a Novel One-Kidney Genetic Model.
Age, Specimen part
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