ReviewImmunologic research2007
Common mechanisms for the regulation of B cell differentiation and transformation by the transcriptional repressor protein BCL-6.
Review in Immunologic research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Contribution of Epstein-Barr Virus Lytic Proteins to Cancer Hallmarks and Implications from Other Oncoviruses.Cancers · 2023Review
- Immunoglobulins and Transcription Factors in Otitis Media.International journal of molecular sciences · 2021Review
- CHD4/NuRD complex regulates complement gene expression and correlates with CD8 T cell infiltration in human hepatocellular carcinoma.Clinical epigenetics · 2020Article
- Suppression of human B cell activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin involves altered regulation of B cell lymphoma-6.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Cancer biology and NuRD: a multifaceted chromatin remodelling complex.Nature reviews. Cancer · 2011Review
- DNA methylation prevents CTCF-mediated silencing of the oncogene BCL6 in B cell lymphomas.The Journal of experimental medicine · 2010Article
- IgA and Differentiation-associated Transcription Factors in Chronic Otitis Media with Effusion.Clinical and experimental otorhinolaryngology · 2009Article
- A human natural killer cell subset provides an innate source of IL-22 for mucosal immunity.Nature · 2009Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The BCL-6 transcriptional repressor protein is a critical regulator of normal B cell differentiation and BCL-6 has recently been shown to act as an oncogene in several mouse model systems. The molecular pathways by which BCL-6 regulates B cell differentiation and also promotes the transformation of primary B cells are undoubtedly related; however, these pathways are poorly understood. The commonly accepted model for BCL-6 function in B cells is that BCL-6 inhibits the terminal differentiation of activated B cells into plasma cells and that deregulation of BCL-6 expression leads to an inhibition of terminal differentiation and continued proliferation. BCL-6 induces a germinal-center phenotype in primary B cells by unknown mechanisms, and can reverse the terminal differentiation of plasma cell tumor lines. BCL-6 can promote the immortalization of primary B cells and can augment telomerase activity. The role of the vast majority of BCL-6 target genes and interacting proteins in normal B cell differentiation and B cell transformation is essentially unresolved and is an important area for future investigation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.