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IgD expressed in nucleus of Pro-B cells promotes Pro-B cells proliferation by regulating E2F3 expression [ChIP-seq]

ABSTRACT: Immunoglobulin D (IgD) has historically been considered as a surface marker of mature B cell with its specific function being undefined. Until now, no evidence had been presented to suggest that IgD is also expressed in pro-B cells. Here, we developed a mouse model with a targeted deletion of IgD, and assessed the production of the IgM, IgG and IgA, as well as the generation of the antigen specific antibodies. The findings indicated no significant differences in these Ig levels between wild type and IgD-deficient mice. However, we observed a notable reduction in the number of mature B cells, which led us to the surprising discovery that this decrease in B cell count begins at the pro-B cell stage. More significantly, we identified that IgD, in its intact tetrapeptide structure, is expressed in the nucleus of pro-B cells. Functionally, IgD appears to promote the proliferation of pro-B cells. Mechanically, IgD exhibits a transcription factor-like activity, and directly binds to the promoter region of E2f3, a pro-proliferative transcription factor. IgD drives the expression of E2f3, thereby promoting the proliferation of pro-B cells. This novel insight into the physiological significance of IgD in B cell development has important implications for our understanding of immune system function.

ORGANISM(S): Mus musculus

PROVIDER: GSE268102 | GEO | 2025/05/22

REPOSITORIES: GEO

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IgD expressed in nucleus of Pro-B cells promotes Pro-B cells proliferation by regulating E2F3 expression [ChIP-seq]

Project description:IgD expressed in nucleus of Pro-B cells promotes Pro-B cells proliferation by regulating E2F3 expression [ChIP-seq]

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Role of IgD in B cell anergy

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Amplification and overexpression of E2F3 in human bladder cancer.

Project description:We demonstrate that, in human bladder cancer, amplification of the E2F3 gene, located at 6p22, is associated with overexpression of its encoded mRNA transcripts and high levels of expression of E2F3 protein. Immunohistochemical analyses of E2F3 protein levels have established that around one-third (33/101) of primary transitional cell carcinomas of the bladder overexpress nuclear E2F3 protein, with the proportion of tumours containing overexpressed nuclear E2F3 increasing with tumour stage and grade. When considered together with the established role of E2F3 in cell cycle progression, these results suggest that the E2F3 gene represents a candidate bladder cancer oncogene that is activated by DNA amplification and overexpression. Keywords: Tumour vs normal comparison, array CGH

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Expression data from lenses triply deficient for E2F1, E2F2, and E2F3 transcription factors

Project description:The E2F family consists of transcriptional repressors and activators that control cell proliferation. In the classic paradigm of cell cycle regulation, the three activators, E2F1, E2F2 and E2F3, are invariably depicted as the final components of a CDK/Rb signaling cascade that executes the transcriptional program necessary to commit cells to enter S phase. Unexpectedly, we find through analysis of Affymetrix expression array data that mature lens epithelial cells deficient for E2F1-3 fail to repress cell cycle-regulated genes (and other targets of E2F) and that this corresponds with subsequent apoptosis and cellular collapse in the lens. Murine lenses were collected at two stages of development for RNA extraction and hybridization on Affymetrix microarrays. Our aim was to determine key events that lead to cellular collapse of lenses triply deficient for E2F1, E2F2, and E2F3 in neonates.

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The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

Project description:The activating E2F-transcription factors are best known for their dependence on the Retinoblastoma protein and their role in cellular proliferation. E2F3 is uniquely amplified in specific human tumours where its expression is inversely correlated with the survival of patients. Here, E2F3 interaction partners were identified by mass spectrometric analysis. We show that the SNF2-like HELLS interacts with E2F3 in vivo and cooperates with its oncogenic functions. Depletion of HELLS severely perturbs the induction of E2F-target genes, hinders cell cycle re-entry and growth. Using chromatin immmunoprecipitation coupled to sequencing we identified genome-wide targets of HELLS and E2F3. Our analysis revealed that HELLS binds near promoters of active genes, including the trithorax-related MLL1, and co-regulates E2F3-dependent genes. Our analysis is the first to link HELLS with E2F-controlled processes that are critical to establish a proliferative tumour circuitry. Strikingly, just as E2F3, HELLS is overexpressed in human tumours including prostate cancer, indicating that either factor may contribute to the malignant progression of tumours. Our work reveals that HELLS is important for E2F3 in tumour cell proliferation. Examination of E2F3, Hells, and H3K27me3 in 2 cell types.

2011-12-19 | E-GEOD-33791 | biostudies-arrayexpress

Role of E2F3 expression in human bladder and prostate cancer cells

Project description:Amplification and overexpression of the E2F3 gene at 6p22 in human bladder cancer is associated with increased tumour stage, grade and proliferation index, and in prostate cancer E2F3 overexpression is linked to tumour aggressiveness. We first used small interfering RNA technology to confirm the potential importance of E2F3 overexpression in bladder cancer development. Knockdown of E2F3 expression in bladder cells containing the 6p22 amplicon strongly reduced the extent of bromodeoxyuridine (BrdU) incorporation and the rate of cellular proliferation. In contrast, knockdown of CDKAL1/ FLJ20342, another proposed oncogene, from this amplicon had no effect. Expression cDNA microarray analysis on bladder cancer cells following E2F3 knockdown was then used to identify genes regulated by E2F3, leading to the identification of known E2F3 targets such as Cyclin A and CDC2 and novel targets including pituitary tumour transforming gene 1, Polo-like kinase 1 (PLK1) and Caveolin-2. For both bladder and prostate cancer, we have proposed that E2F3 protein overexpression may cooperate with removal of the E2F inhibitor retinoblastoma tumor suppressor protein (pRB) to drive cellular proliferation. In support of this model, we found that ectopic expression of E2F3a enhanced the BrdU incorporation, a marker of cellular proliferation rate, of prostate cancer DU145 cells, which lack pRB, but had no effect on the proliferation rate of PC3 prostate cancer cells that express wild-type pRB. BrdU incorporation in PC3 cells could, however, be increased by overexpressing E2F3a in cells depleted of pRB. When taken together, these observations indicate that E2F3 levels have a critical role in modifying cellular proliferation rate in human bladder and prostate cancer. Keywords: siRNA knock down

2006-10-28 | GSE6131 | GEO

The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

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