Mus musculus domesticus strain:BALB/c
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1251130 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR33989006_1.fastq.gz | Fastqsanger.gz | |||
| SRR33989006_2.fastq.gz | Fastqsanger.gz | |||
| SRR33989008_1.fastq.gz | Fastqsanger.gz | |||
| SRR33989008_2.fastq.gz | Fastqsanger.gz |
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Project description:BLIMP1 controls GC B cell expansion and exit through regulating cell cycle progression and key transcription factors BCL6 and IRF4
| PRJNA1050777 | ENA
Project description:In B cells BLIMP1 is required for plasma cell differentiation. BLIMP1 is also expressed in some dark zone (DZ) germinal center (GC) B cells (GCBCs), yet the role of BLIMP1 in GCBCs is not understood. Here we generated mixed bone marrow (BM) chimeric mice using Prdm1+/+ CD19Cre and Prdm1fl/fl CD19Cre BM, allowing us to examine the cell-intrinsic functions of BLIMP1 in GCBC, independent of antibody or antigen levels. Strikingly, BLIMP1-deficient B cells quickly dominate GCs and persist for a much longer time compared to the wild type cells. BLIMP1 deficiency promotes positive selection of GCBC and enhances cell-cycle progression. In addition, BLIMP1 deficiency enhanced class-switching. Mechanistically, BLIMP1-deficient GCBC fail to downregulate BCL6 and to upregulate IRF4, indicating that BLIMP1 controls the expression of these transcription factors that mediate exit from the GC. These studies revealed unique functions of BLIMP1 in regulating GCBC responses that impact long-lived immune compartments.
2024-03-28 | GSE249811 | GEO
Project description:Background: Germinal center B-cell (GCB) lymphomas are common in children and adults. The prognosis strongly depends on age. Subgroups of GCB-lymphomas are characterized by chromosomal translocations affecting immunoglobulin (IG) loci leading to oncogene deregulation. Methods: Novel IG translocation partners were cloned within the network “Molecular Mechanisms in Malignant Lymphomas” (MMML) by long-distance inverse polymerase chain reaction. Mature aggressive B-cell lymphomas from the MMML as well as pediatric and adult lymphoma trials were analyzed by fluorescence in situ hybridization (FISH) and immunhistochemistry. Data from 438 MMML cases characterized by gene expression profiling were mined. Results: Cloning of unknown IG partners identified a t(6;14)(p25;q32) juxtaposing the IRF4 oncogene with the IGH-locus as novel recurrent aberration in GCB lymphoma. FISH analyses of 427 mature B-cell lymphomas for IRF4 translocations revealed 20 IG/IRF4 positive lymphomas (17 IGH/IRF4, 2 IGL/IRF4, 1 IGΚ/IRF4). IG/IRF4-positive lymphomas were predominantly GCB-type diffuse large B-cell lymphomas (DLBCL) or follicular lymphoma grade 3, shared overexpression of IRF4/MUM1 and BCL6 and lacked PRDM1/BLIMP1 expression and t(14;18)/BCL2 breaks. BCL6 aberrations were common. The gene expression profile of IG/IRF4-positive lymphomas was different from other subtypes of DLBCL and a classifier for IG/IRF4 positivity containing 27 genes allowed prediction of 3 additional MMML IG/IRF4-positive cases subsequently proven by FISH. IG/IRF4-positivity was associated with a favorable outcome likely due to significant enrichment of IG/IRF4-positive lymphomas in childhood and young adulthood. Conclusions: Our results suggest IRF4 translocations to be primary genetic alterations in a novel molecularly defined subset of GC-derived lymphomas predominantly affecting children. 271 diffuse large B-Cell lymphoma samples were hybridized to HGU133A Affymetrix GeneChips.
2011-06-24 | E-GEOD-22470 | biostudies-arrayexpress
Project description:OBF1 is a specific coactivator of the POU family transcription factors OCT1 and OCT2. OBF1 and OCT2 are B cell-specific and indispensable for germinal center (GC) formation, but their mechanism of action is unclear. Here, we show by ChIP-seq that OBF1 extensively colocalizes with OCT1 and OCT2 and stabilizes their binding. We found that these factors also often colocalize with transcription factors of the ETS family, such as PU.1 and ETS1. Furthermore, we showed that OBF1, OCT2 and OCT1 bind widely to the promoters or enhancers of genes involved in GC formation, such as the master regulators Bcl6 and Foxo1. shRNA knockdown experiments demonstrated that OCT1, OCT2 and OBF1 are essential for proliferation of GC-derived lymphoma cell lines. OBF1 downregulation disrupts the GC transcriptional program: genes involved in GC maintenance -such as BCL6- are downregulated, while genes related to exit from the GC program are upregulated. Ectopic expression of BCL6 does not restore the proliferation of GC-derived Raji cells depleted of OBF1 unless IRF4 is also depleted, indicating that OBF1 controls a critical regulatory node in GC differentiation.
2021-02-02 | GSE161837 | GEO
Project description:OBF1 is a specific coactivator of the POU family transcription factors OCT1 and OCT2. OBF1 and OCT2 are B cell-specific and indispensable for germinal center (GC) formation, but their mechanism of action is unclear. Here, we show by ChIP-seq that OBF1 extensively colocalizes with OCT1 and OCT2 and stabilizes their binding. We found that these factors also often colocalize with transcription factors of the ETS family, such as PU.1 and ETS1. Furthermore, we showed that OBF1, OCT2 and OCT1 bind widely to the promoters or enhancers of genes involved in GC formation, such as the master regulators Bcl6 and Foxo1. shRNA knockdown experiments demonstrated that OCT1, OCT2 and OBF1 are essential for proliferation of GC-derived lymphoma cell lines. OBF1 downregulation disrupts the GC transcriptional program: genes involved in GC maintenance -such as BCL6- are downregulated, while genes related to exit from the GC program are upregulated. Ectopic expression of BCL6 does not restore the proliferation of GC-derived Raji cells depleted of OBF1 unless IRF4 is also depleted, indicating that OBF1 controls a critical regulatory node in GC differentiation.
2021-02-02 | GSE142037 | GEO
Project description:OBF1 is a specific coactivator of the POU family transcription factors OCT1 and OCT2. OBF1 and OCT2 are B cell-specific and indispensable for germinal center (GC) formation, but their mechanism of action is unclear. Here, we show by ChIP-seq that OBF1 extensively colocalizes with OCT1 and OCT2 and stabilizes their binding. We found that these factors also often colocalize with transcription factors of the ETS family, such as PU.1 and ETS1. Furthermore, we showed that OBF1, OCT2 and OCT1 bind widely to the promoters or enhancers of genes involved in GC formation, such as the master regulators Bcl6 and Foxo1. shRNA knockdown experiments demonstrated that OCT1, OCT2 and OBF1 are essential for proliferation of GC-derived lymphoma cell lines. OBF1 downregulation disrupts the GC transcriptional program: genes involved in GC maintenance -such as BCL6- are downregulated, while genes related to exit from the GC program are upregulated. Ectopic expression of BCL6 does not restore the proliferation of GC-derived Raji cells depleted of OBF1 unless IRF4 is also depleted, indicating that OBF1 controls a critical regulatory node in GC differentiation.
2021-02-02 | GSE142039 | GEO
Project description:OBF1 is a specific coactivator of the POU family transcription factors OCT1 and OCT2. OBF1 and OCT2 are B cell-specific and indispensable for germinal center (GC) formation, but their mechanism of action is unclear. Here, we show by ChIP-seq that OBF1 extensively colocalizes with OCT1 and OCT2 and stabilizes their binding. We found that these factors also often colocalize with transcription factors of the ETS family, such as PU.1 and ETS1. Furthermore, we showed that OBF1, OCT2 and OCT1 bind widely to the promoters or enhancers of genes involved in GC formation, such as the master regulators Bcl6 and Foxo1. shRNA knockdown experiments demonstrated that OCT1, OCT2 and OBF1 are essential for proliferation of GC-derived lymphoma cell lines. OBF1 downregulation disrupts the GC transcriptional program: genes involved in GC maintenance -such as BCL6- are downregulated, while genes related to exit from the GC program are upregulated. Ectopic expression of BCL6 does not restore the proliferation of GC-derived Raji cells depleted of OBF1 unless IRF4 is also depleted, indicating that OBF1 controls a critical regulatory node in GC differentiation.
2021-02-02 | GSE142038 | GEO
Project description:OBF1 is a specific coactivator of the POU family transcription factors OCT1 and OCT2. OBF1 and OCT2 are B cell-specific and indispensable for germinal center (GC) formation, but their mechanism of action is unclear. Here, we show by ChIP-seq that OBF1 extensively colocalizes with OCT1 and OCT2 and stabilizes their binding. We found that these factors also often colocalize with transcription factors of the ETS family, such as PU.1 and ETS1. Furthermore, we showed that OBF1, OCT2 and OCT1 bind widely to the promoters or enhancers of genes involved in GC formation, such as the master regulators Bcl6 and Foxo1. shRNA knockdown experiments demonstrated that OCT1, OCT2 and OBF1 are essential for proliferation of GC-derived lymphoma cell lines. OBF1 downregulation disrupts the GC transcriptional program: genes involved in GC maintenance -such as BCL6- are downregulated, while genes related to exit from the GC program are upregulated. Ectopic expression of BCL6 does not restore the proliferation of GC-derived Raji cells depleted of OBF1 unless IRF4 is also depleted, indicating that OBF1 controls a critical regulatory node in GC differentiation.
2021-02-02 | GSE161840 | GEO
Project description:OBF1 is a specific coactivator of the POU family transcription factors OCT1 and OCT2. OBF1 and OCT2 are B cell-specific and indispensable for germinal center (GC) formation, but their mechanism of action is unclear. Here, we show by ChIP-seq that OBF1 extensively colocalizes with OCT1 and OCT2 and stabilizes their binding. We found that these factors also often colocalize with transcription factors of the ETS family, such as PU.1 and ETS1. Furthermore, we showed that OBF1, OCT2 and OCT1 bind widely to the promoters or enhancers of genes involved in GC formation, such as the master regulators Bcl6 and Foxo1. shRNA knockdown experiments demonstrated that OCT1, OCT2 and OBF1 are essential for proliferation of GC-derived lymphoma cell lines. OBF1 downregulation disrupts the GC transcriptional program: genes involved in GC maintenance -such as BCL6- are downregulated, while genes related to exit from the GC program are upregulated. Ectopic expression of BCL6 does not restore the proliferation of GC-derived Raji cells depleted of OBF1 unless IRF4 is also depleted, indicating that OBF1 controls a critical regulatory node in GC differentiation.
2021-02-02 | GSE161838 | GEO
Project description:Humoral immunity requires the generation of high-affinity antibodies, which involves the generation of germinal centres (GC) promoting class switch and affinity maturation of antigen-specific B cells, and the differentiation of long-lived plasma cells. This multi-layered process is tightly controlled by the activity of a transcriptional network including Bcl6, essential for the development of GC, and Blimp1, required for the differentiation of plasma cells. Here, we reveal an additional layer of complexity by demonstrating that dynamic changes in E-protein activity mediated by Id3 govern both GC and plasma cell differentiation. We show that down-regulation of Id3 expression in B cells in essential for releasing E2A and E2-2, the combined activity of which is required for both GC B cell and plasma cell differentiation. We demonstrate that this pathway controls the expression of multiple key factors required for antigen-induced B cell differentiation, including Blimp1, Xbp1, Mef2b and CXCR4 and is therefore critical for establishing the transcriptional network that controls GC B cell and plasma cell differentiation. Genome binding of transcription factor E2A
2016-05-13 | E-GEOD-72828 | biostudies-arrayexpress