Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

62 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of chicken Pax5 deficient DT40 B cell line

ABSTRACT: PAx5 is indispensible for the committment if early lymphoid progenitors to the B cell lineage as well as for the development and maintenance of B cells. To better understand the functional importance of Pax5 in the later stages of B cell development and investigate the targets of Pax5 regulation, we established a novel Pax5 deficient DT40 B cell line.

ORGANISM(S): Gallus gallus

SUBMITTER: Pekka Kohonen

PROVIDER: E-MEXP-270 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Loss of Pax5 promotes plasma cell differentiation.

Nera Kalle-Pekka KP Kohonen Pekka P Narvi Elli E Peippo Anne A Mustonen Laura L Terho Perttu P Koskela Kimmo K Buerstedde Jean-Marie JM Lassila Olli O

Immunity 20060301 3

Pax5 is indispensable for the commitment of early lymphoid progenitors to the B cell lineage as well as for the development of B cells. To better understand the functional importance of Pax5 at the later stages of B cell differentiation, we established a Pax5-deficient DT40 B cell line. The Pax5(-/-) cells exhibited slower growth, decreased surface IgM expression, and total loss of B cell receptor signaling. Moreover, the expression of the plasma cell-characteristic transcription factors Blimp-1 ...[more]

PMID: 16546097

Similar Datasets

Cross-species meta-analysis of regulatory networks of the Pax5 transcription factor

Project description:Transcription profiling of chicken Pax5 deficient DT40 B cell line to investigate the targets of Pax5 which is required for B-cell differentiation Used in cross-species comparison to investigate evolutionarily conserved regulatory circuits in B cell development Pax5 deficient DT40 B cells (3 biological replicates) were compared to DT40 wild-type cells (3 biological replicates).

2013-12-31 | E-GEOD-34687 | biostudies-arrayexpress

Transcription profiling of chicken Bcl6 deficient DT40 B cell line to investigate the targets of Bcl6 which is required for germinal center formation

Project description:The transcription factor Bcl6 is required for germinal center formation and deregulated expression of Bcl6 has been observed in lymphomas. To gain insight to the function of Bcl6 in terminal differentiation of B cells to plasma cells and to investigate the targets of Bcl6, we established a Bcl6 deficient DT40 B cell line.

2010-02-17 | E-MEXP-2062 | biostudies-arrayexpress

PAX5 overexpression is not enough to reestablish the mature B-cell phenotype in classical Hodgkin lymphoma (ChIP-Seq)

Project description:In lymphomas derived from mature B cells the expression of the transcription factor PAX5 is maintained whereas classical Hodgkin lymphoma displays significantly reduced PAX5 expression despite its derivation from mature B cells. To elucidate the functional role of PAX5 in classical Hodgkin lymphoma, we re-established the PAX5 expression in the Hodgkin cell line L428 with and without epigenetic modulation. To this end, we stably transfected the Hodgkin cell line L428 with an inducible PAX5 expression construct. Although the overexpressed PAX5 was transcriptionally active as demonstrated by synthetic reporter constructs, no induction of the B-cell phenotype was achieved. PAX5 chromatin immunoprecipitation with subsequent next generation sequencing in B-cell lines and the PAX5 overexpressing L428 cell line showed different binding patterns. Since epigenetic restrictions might affect PAX5 binding, combined DNA demethylation and histone acetylation was performed. However, no re-expression of B-cell genes was observed also under these conditions. Thus, PAX5 is not sufficient for the re-activation of the B-cell program in Hodgkin cells despite epigenetic opening of the chromatin. This clearly indicates that the repression of the B-cell identity of the Hodgkin cells is caused and secured by complex molecular mechanisms. Analysis of genome-wide PAX5 binding sites in B-cell lines (Raji, Namalwa) and the PAX5-producing Hodgkin cell line L428-PAX5 by ChIP-Seq

2013-07-30 | E-GEOD-44551 | biostudies-arrayexpress

PAX5 overexpression is not enough to reestablish the mature B-cell phenotype in classical Hodgkin lymphoma

Project description:In lymphomas derived from mature B cells the expression of the transcription factor PAX5 is maintained whereas classical Hodgkin lymphoma displays significantly reduced PAX5 expression despite its derivation from mature B cells. To elucidate the functional role of PAX5 in classical Hodgkin lymphoma, we re-established the PAX5 expression in the Hodgkin cell line L428 with and without epigenetic modulation. To this end, we stably transfected the Hodgkin cell line L428 with an inducible PAX5 expression construct. Although the overexpressed PAX5 was transcriptionally active as demonstrated by synthetic reporter constructs, no induction of the B-cell phenotype was achieved. PAX5 chromatin immunoprecipitation with subsequent next generation sequencing in B-cell lines and the PAX5 overexpressing L428 cell line showed different binding patterns. Since epigenetic restrictions might affect PAX5 binding, combined DNA demethylation and histone acetylation was performed. However, no re-expression of B-cell genes was observed also under these conditions. Thus, PAX5 is not sufficient for the re-activation of the B-cell program in Hodgkin cells despite epigenetic opening of the chromatin. This clearly indicates that the repression of the B-cell identity of the Hodgkin cells is caused and secured by complex molecular mechanisms. 2 Burkitt lymphoma cell lines (Raji, Namalwa), the Hodgkin lymphoma cell line L428 and the PAX5-producing L428 (L428-PAX5) with or without 5-aza-2M-bM-^@M-2-deoxycytidine/Trichostatin A treatment were analysed in triplicate.

2013-07-30 | E-GEOD-44244 | biostudies-arrayexpress

Transcription profiling of mouse Pax5-/- proB cells transduced with control or EBF retrovirus.

Project description:We have determined that sustained expression of EBF suppresses alternate lineage genes independently of Pax5. Experiment Overall Design: Pax5-/- pro-B cells transduced with control or EBF retrovirus. Transduced cells were FACS sorted based on GFP expression and total RNA was isolated. RNA isolated from control or EBF transduced cells was analyzed using the Affymetrix Rat 230A microarrays.

2008-06-16 | E-GEOD-9878 | biostudies-arrayexpress

Concerted action of Helios and Ikaros balances the strength of B cell receptor signaling and controls the expression of inositol 5-phosphatase SHIP

Project description:Inositol 5-phosphatase SHIP is differentially expressed in Ikaros and Helios deficient cells. In the absense of Ikaros SHIP is upregulated where as in the absense of Helios it is downregulated. Ikaros binds to the promoter of the SHIP gene. Article provides insight into the mechanisms of action Ikaros employs to regulate BCR signaling. Two replicates of Ikaros deficient and wild type DT40 avian B cells.

2010-07-19 | E-GEOD-20946 | biostudies-arrayexpress

Chip-chip from pro-B cells with H3K4me3, H3K4me2 and H3K9ac

Project description:The transcription factor Pax5 represses B-lineage-inappropriate genes and activates B-cell-specific genes in B-lymphocytes. Here we have identified 170 novel Pax5-activated genes. Conditional mutagenesis demonstrated that the Pax5-regulated genes require continuous Pax5 activity for normal expression in pro-B and mature B cells. Expression of half of the Pax5-activated genes is either absent or significantly reduced upon Pax5 loss in plasma cells. Direct Pax5 target genes were identified based on their protein synthesis-independent activation by a Pax5-estrogen receptor fusion protein. Chromatin immunoprecipitation (ChIP) of Pax5 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Pax5 directly activates the chromatin at promoters or putative enhancers of Pax5 target genes. The novel Pax5-activated genes code for key regulatory and structural proteins involved in B cell signaling, adhesion, migration, antigen presentation and germinal center B cell formation, thus revealing a complex regulatory network, which is activated by Pax5 to control B cell development and function. Keywords: Chip-chip, cell type comparison comparison of Pax5-/-Rag2-/- vs Rag2-/- pro-B cells

2010-05-20 | E-GEOD-15145 | biostudies-arrayexpress

Chip-chip from pro-B cells with H3K4me3, H3K4me2 and H3K9ac

2007-08-23 | E-GEOD-8472 | biostudies-arrayexpress

Genome-wide binding map of FoxO1 and Pax5 in pre-B cells

Project description:Genome-wide analysis of FoxO1 and Pax5 binding in pre-B cells following attenuation of IL-7 signaling. Transcription factor FoxO1 has been shown to be an essential factor for Ig light chain rearrangement. Results demonstrate that FoxO1 and Pax5 co-target genes that are activated during pre-B cell differentiation. Examination of FoxO1 and/or Pax5 binding under withdrawal of IL-7R signaling.

2012-01-12 | E-GEOD-35024 | biostudies-arrayexpress

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data