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Aryl Hydrocarbon Receptor Interacting Protein Maintains Germinal Center B Cells through Suppression of BCL6 Degradation

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Title: Aryl Hydrocarbon Receptor Interacting Protein Maintains Germinal Center B Cells through Suppression of BCL6 Degradation
Authors: Dijue Sun, Urszula Stopka-Farooqui, Sayka Barry, Ezra Aksoy, Gregory Parsonage, Anna Vossenkämper, Melania Capasso, Xinyu Wan, Sherine Norris, Jennifer L. Marshall, Andrew Clear, John Gribben, Thomas T. MacDonald, Christopher D. Buckley, Márta Korbonits, Oliver Haworth
Source: Cell Reports, Vol 27, Iss 5, Pp 1461-1471.e4 (2019)
Publisher Information: Elsevier, 2019.
Publication Year: 2019
Collection: LCC:Biology (General)
Subject Terms: Biology (General), QH301-705.5
More Details: Summary: B cell lymphoma-6 (BCL6) is highly expressed in germinal center B cells, but how its expression is maintained is still not completely clear. Aryl hydrocarbon receptor interacting protein (AIP) is a co-chaperone of heat shock protein 90. Deletion of Aip in B cells decreased BCL6 expression, reducing germinal center B cells and diminishing adaptive immune responses. AIP was required for optimal AKT signaling in response to B cell receptor stimulation, and AIP protected BCL6 from ubiquitin-mediated proteasomal degradation by the E3-ubiquitin ligase FBXO11 by binding to the deubiquitinase UCHL1, thus helping to maintain the expression of BCL6. AIP was highly expressed in primary diffuse large B cell lymphomas compared to healthy tissue and other tumors. Our findings describe AIP as a positive regulator of BCL6 expression with implications for the pathobiology of diffuse large B cell lymphoma. : BCL6 overexpression contributes to the pathobiology of diffuse large B cell lymphoma (DLBCL). Sun et al. find that the co-chaperone aryl hydrocarbon receptor interacting protein (AIP), whose high expression is associated with reduced survival of DLBCL patients, helps maintain BCL6 expression by facilitating the removal of ubiquitin from BCL6. Keywords: AIP, BCL6, FBXO11, UCHL1, ubiquitination, lymphoma
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2211-1247
Relation: http://www.sciencedirect.com/science/article/pii/S2211124719304693; https://doaj.org/toc/2211-1247
DOI: 10.1016/j.celrep.2019.04.014
Access URL: https://doaj.org/article/0e7c48760a0e4810870ae935225004a8
Accession Number: edsdoj.0e7c48760a0e4810870ae935225004a8
Database: Directory of Open Access Journals
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  Data: Aryl Hydrocarbon Receptor Interacting Protein Maintains Germinal Center B Cells through Suppression of BCL6 Degradation
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  Data: Cell Reports, Vol 27, Iss 5, Pp 1461-1471.e4 (2019)
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  Data: Elsevier, 2019.
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  Data: Summary: B cell lymphoma-6 (BCL6) is highly expressed in germinal center B cells, but how its expression is maintained is still not completely clear. Aryl hydrocarbon receptor interacting protein (AIP) is a co-chaperone of heat shock protein 90. Deletion of Aip in B cells decreased BCL6 expression, reducing germinal center B cells and diminishing adaptive immune responses. AIP was required for optimal AKT signaling in response to B cell receptor stimulation, and AIP protected BCL6 from ubiquitin-mediated proteasomal degradation by the E3-ubiquitin ligase FBXO11 by binding to the deubiquitinase UCHL1, thus helping to maintain the expression of BCL6. AIP was highly expressed in primary diffuse large B cell lymphomas compared to healthy tissue and other tumors. Our findings describe AIP as a positive regulator of BCL6 expression with implications for the pathobiology of diffuse large B cell lymphoma. : BCL6 overexpression contributes to the pathobiology of diffuse large B cell lymphoma (DLBCL). Sun et al. find that the co-chaperone aryl hydrocarbon receptor interacting protein (AIP), whose high expression is associated with reduced survival of DLBCL patients, helps maintain BCL6 expression by facilitating the removal of ubiquitin from BCL6. Keywords: AIP, BCL6, FBXO11, UCHL1, ubiquitination, lymphoma
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  Data: http://www.sciencedirect.com/science/article/pii/S2211124719304693; https://doaj.org/toc/2211-1247
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