Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Enhancer retargeting at the PAX5/ZCCHC7 locus

ABSTRACT: 2 kinds of SU-DHL-10 cell clones (Pax5-TSS2mut/deletion) were generated to investigate enhancer relocation, we campared 4C-seq data between the Pax5-TSS2mut/deletion clones and wild type SU-DHL-10.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210888 | GEO | 2023/09/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genes expression of SU-DHL-2 cells treated with IL-17A

Project description:To further figure out the molecular mechanisms of IL-17A-mediated DLBCL cells growth, we used the Whole Human Genome Oligo Microarray (4×44K, Agilent Technologies) to identify genes expression. Six samples of SU-DHL-2 cells (2×10^6 cells/ml) co-cultured with or without IL-17A (200pg/ml) for 72hr in vivo. Three samples of SU-DHL-2 cells were all co-cultured with IL-17A , other three samples of SU-DHL-2 cells without IL-17A treatment were used as controls. Then, all these six samples of SU-DHL-2 cells were measured by microarray.

2018-06-16 | GSE115855 | GEO

Proteomes of chromatin fractions derived from SU-DHL-5 cells

Project description:SU-DHL-5 cells display limited expression of the SUMO isopeptidase SENP6. In this experiment, the chromatin associated fraction of SU-DHL-5 cells was analysed by mass spectrometry. SU-DHL-5 cells were either stably transfected with an empty vector or with a SENP6 expression construct. Changes in protein levels were compared between these two cell lines in triplicate experiments.

2022-02-17 | PXD027355 | Pride

ena-DATASET-DKFZ-IBIOS-17-08-2015-09:13:01:216-19 - samples

Project description:PAR-CLIP was performed on the Argonaute-2 protein (AGO2) in four lymphoma cell lines: Namalwa Raji SU-DHL-4 SU-DHL-6

| EGAD00001001468 | EGA

Germline Aberrations of PAX5 Cause Susceptibility to pre-B cell Acute Lymphoblastic Leukemia

Project description:A novel heterozygous germline variant, c.547G>A (p.Gly183Ser), in the paired box protein encoding gene, PAX5, was found to segregate with disease in two unrelated kindreds with autosomal dominant pre-B cell acute lymphoblastic leukemia (ALL). Leukemic cells from both families exhibited 9p deletion, with loss-of-heterozygosity and retention of the mutant PAX5 allele at 9p13. Two additional sporadic ALL cases with 9p loss demonstrated PAX5 Gly183 substitution in the leukemic cells. Functional and gene expression analysis of the PAX5 germline variants demonstrated reduced transcriptional activity. These data extend the role of PAX5 alterations in the pathogenesis of pre-B ALL, and implicate PAX5 in a novel syndrome of germline susceptibility to pre-B cell neoplasia. We analyzed 10 samples of J558 murine myeloma cells infected with MSCV-Puro-IRES-GFP (PIG) empty vector (EV; three independent replicates), MSCV-PIG Pax5 WT (WT; three independent replicates), and MSCV-PIG Pax5 G183S (Mut; four independent replicates). Cells were selected with puromycin after infection for 5-7 days, subsequently cells were sorted for GFP and IgM expression by FACS.

2014-04-06 | E-GEOD-45834 | biostudies-arrayexpress

PAX5 transduction of Pax5-/- pro-B cells

Project description:PAX5 transduction of Pax5-/- pro-B cells

| PRJNA414096 | ENA

Germline Aberrations of PAX5 Cause Susceptibility to pre-B cell Acute Lymphoblastic Leukemia

Project description:A novel heterozygous germline variant, c.547G>A (p.Gly183Ser), in the paired box protein encoding gene, PAX5, was found to segregate with disease in two unrelated kindreds with autosomal dominant pre-B cell acute lymphoblastic leukemia (ALL). Leukemic cells from both families exhibited 9p deletion, with loss-of-heterozygosity and retention of the mutant PAX5 allele at 9p13. Two additional sporadic ALL cases with 9p loss demonstrated PAX5 Gly183 substitution in the leukemic cells. Functional and gene expression analysis of the PAX5 germline variants demonstrated reduced transcriptional activity. These data extend the role of PAX5 alterations in the pathogenesis of pre-B ALL, and implicate PAX5 in a novel syndrome of germline susceptibility to pre-B cell neoplasia. We analyzed 40 samples comprising sevenfold replicates of transductions with empty vector, wild type PAX5 and 4 mutant PAX5 constructs

2013-08-01 | E-GEOD-45260 | biostudies-arrayexpress

Gene expression analysis of Hodgkin and non-Hodgkin lymphoma cell lines

Project description:Genomewide gene expression analysis of lymphoid cell lines of Hodgkin, non-Hodgkin and acute leukemia origin Affymetrix U133 Plus 2.0 oligonucleotide arrays were hybridized to determine the gene expression profile of Hodgkin (L428, L1236, KM-H2, HDLM-2, L540, L540Cy), non-Hodgkin (Namalwa, SU-DHL-4) and acute lymphoblastic leukemia (Reh) cell lines; all hybridizations were done in biological duplicates (except L540, L50Cy, SU-DHL-4).

2010-11-17 | E-GEOD-20011 | biostudies-arrayexpress

Essential role of the Pax5 C-terminal domain in controlling B cell commitment and development

Project description:The B-cell regulator Pax5 consists of multiple domains, whose function we analyzed in vivo by deletion in Pax5. While B-lymphopoiesis was minimally affected in mice with homozygous deletion of the octapeptide or partial homeodomain, both sequences were required for optimal B-cell development. Deletion of the C-terminal regulatory domain 1 (CRD1) interfered with B-cell development, while elimination of CRD2 modestly affected B-lymphopoiesis. Deletion of CRD1 and CRD2 arrested B-cell development at an uncommitted pro-B cell stage. Most Pax5-regulated genes required CRD1 or both CRD1 and CRD2 for their activation or repression, as these domains induced or eliminated open chromatin at Pax5-activated or Pax5-repressed genes, respectively. Co-immunoprecipitation experiments demonstrated that the activating function of CRD1 is mediated through interaction with the chromatin-remodeling BAF, H3K4-methylating Set1A-COMPASS and H4K16-acetylating NSL complexes, while its repressing function depends on recruitment of the Sin3-HDAC and MiDAC complexes. These data provide novel molecular insight into how different Pax5 domains regulate gene expression to promote B-cell commitment and development.

2023-08-24 | GSE224793 | GEO

Essential role of the Pax5 C-terminal domain in controlling B cell commitment and development

Project description:Pax5 controls B-cell commitment, development and immunity by repressing B-lineage-inappropriate genes and activating B-cell-specific genes. In addition to the N-terminal DNA-binding paired domain, Pax5 contains a conserved octapeptide, partial homeodomain and C-terminal sequences with transactivating and inhibitory potential. To understand how the C-terminal domains of Pax5 contribute to the repression and activation function of Pax5, we performed Pax5 pulldown combined with mass spectrometry to identify coactivator or corepressor complexes that bind to the C-terminal regions of Pax5.

2023-08-24 | PXD040424 | Pride

Germline Aberrations of PAX5 Cause Susceptibility to pre-B cell Acute Lymphoblastic Leukemia

2013-08-01 | GSE45260 | GEO