Overexpression of Bcl-3 inhibits the development of marginal zone B cells

Publikationstyp:
Zeitschriftenaufsatz
Metadaten:
Autoren
  • Nadine Hoevelmeyer
  • Marcus A Woerns
  • Sonja Reissig
  • Petra Adams-Quack
  • Jennifer Leclaire
  • Matthias Hahn
  • Simone Woertge
  • Alexei Nikolaev
  • Peter R Galle
  • Ari Waisman
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000331901200024&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.1002/eji.201343655
eISSN
1521-4141
Externe Identifier
  • Clarivate Analytics Document Solution ID: AB6LX
  • PubMed Identifier: 24242374
ISSN
0014-2980
Ausgabe der Veröffentlichung
2
Zeitschrift
EUROPEAN JOURNAL OF IMMUNOLOGY
Schlüsselwörter
  • B-1 B cells
  • Bcl-3
  • Marginal zone B cell
  • NF-B
Paginierung
545 - 552
Datum der Veröffentlichung
2014
Status
Published
Titel
Overexpression of Bcl-3 inhibits the development of marginal zone B cells
Sub types
  • Article
Ausgabe der Zeitschrift
44

Datenquelle: Web of Science (Lite)

Andere Metadatenquellen:
Abstract
<jats:p>The transcription factor Bcl‐3 functions as a proto‐oncogene via regulation of cell proliferation and apoptosis. Bcl‐3 is an atypical member of the IκB family and plays a central role in the immune response through interactions with the NF‐κB subunits p50 and p52. To investigate the impact of Bcl‐3 on B‐cell maturation and regulation, we generated mice that overexpress Bcl‐3 specifically in B cells. Interestingly, these mice lack marginal zone B cells and exhibit a significant reduction in the number of B‐1 B cells. Further, B cells from these mice are impaired in their proliferative capacity. Our data demonstrate that the overexpression of the transcription factor Bcl‐3 inhibits germinal center formation, marginal zone B‐cell development, and affects the B‐1 B‐cell compartment.</jats:p>
Autoren
  • Nadine Hövelmeyer
  • Marcus A Wörns
  • Sonja Reissig
  • Petra Adams‐Quack
  • Jennifer Leclaire
  • Matthias Hahn
  • Simone Wörtge
  • Alexei Nikolaev
  • Peter R Galle
  • Ari Waisman
DOI
10.1002/eji.201343655
eISSN
1521-4141
ISSN
0014-2980
Ausgabe der Veröffentlichung
2
Zeitschrift
European Journal of Immunology
Sprache
en
Online publication date
2013
Paginierung
545 - 552
Datum der Veröffentlichung
2014
Status
Published
Herausgeber
Wiley
Herausgeber URL
http://dx.doi.org/10.1002/eji.201343655
Datum der Datenerfassung
2023
Titel
Overexpression of Bcl‐3 inhibits the development of marginal zone B cells
Ausgabe der Zeitschrift
44

Datenquelle: Crossref

Abstract
The transcription factor Bcl-3 functions as a proto-oncogene via regulation of cell proliferation and apoptosis. Bcl-3 is an atypical member of the IκB family and plays a central role in the immune response through interactions with the NF-κB subunits p50 and p52. To investigate the impact of Bcl-3 on B-cell maturation and regulation, we generated mice that overexpress Bcl-3 specifically in B cells. Interestingly, these mice lack marginal zone B cells and exhibit a significant reduction in the number of B-1 B cells. Further, B cells from these mice are impaired in their proliferative capacity. Our data demonstrate that the overexpression of the transcription factor Bcl-3 inhibits germinal center formation, marginal zone B-cell development, and affects the B-1 B-cell compartment.
Addresses
  • Institute for Molecular Medicine, Johannes Gutenberg-University of Mainz, Mainz, Germany.
Autoren
  • Nadine Hövelmeyer
  • Marcus A Wörns
  • Sonja Reissig
  • Petra Adams-Quack
  • Jennifer Leclaire
  • Matthias Hahn
  • Simone Wörtge
  • Alexei Nikolaev
  • Peter R Galle
  • Ari Waisman
DOI
10.1002/eji.201343655
eISSN
1521-4141
Externe Identifier
  • PubMed Identifier: 24242374
Open access
false
ISSN
0014-2980
Ausgabe der Veröffentlichung
2
Zeitschrift
European journal of immunology
Schlüsselwörter
  • Germinal Center
  • B-Lymphocytes
  • Animals
  • Mice
  • Proto-Oncogene Proteins
  • Transcription Factors
  • Cell Proliferation
  • Gene Expression
  • B-Cell Lymphoma 3 Protein
Sprache
eng
Medium
Print-Electronic
Online publication date
2013
Paginierung
545 - 552
Datum der Veröffentlichung
2014
Status
Published
Datum der Datenerfassung
2013
Titel
Overexpression of Bcl-3 inhibits the development of marginal zone B cells.
Sub types
  • Research Support, Non-U.S. Gov't
  • Journal Article
Ausgabe der Zeitschrift
44

Datenquelle: Europe PubMed Central

Abstract
The transcription factor Bcl-3 functions as a proto-oncogene via regulation of cell proliferation and apoptosis. Bcl-3 is an atypical member of the IκB family and plays a central role in the immune response through interactions with the NF-κB subunits p50 and p52. To investigate the impact of Bcl-3 on B-cell maturation and regulation, we generated mice that overexpress Bcl-3 specifically in B cells. Interestingly, these mice lack marginal zone B cells and exhibit a significant reduction in the number of B-1 B cells. Further, B cells from these mice are impaired in their proliferative capacity. Our data demonstrate that the overexpression of the transcription factor Bcl-3 inhibits germinal center formation, marginal zone B-cell development, and affects the B-1 B-cell compartment.
Date of acceptance
2013
Autoren
  • Nadine Hövelmeyer
  • Marcus A Wörns
  • Sonja Reissig
  • Petra Adams-Quack
  • Jennifer Leclaire
  • Matthias Hahn
  • Simone Wörtge
  • Alexei Nikolaev
  • Peter R Galle
  • Ari Waisman
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/24242374
DOI
10.1002/eji.201343655
eISSN
1521-4141
Ausgabe der Veröffentlichung
2
Zeitschrift
Eur J Immunol
Schlüsselwörter
  • B-1 B cells
  • Bcl-3
  • Marginal zone B cell
  • NF-κB
  • Animals
  • B-Cell Lymphoma 3 Protein
  • B-Lymphocytes
  • Cell Proliferation
  • Gene Expression
  • Germinal Center
  • Mice
  • Proto-Oncogene Proteins
  • Transcription Factors
Sprache
eng
Country
Germany
Paginierung
545 - 552
Datum der Veröffentlichung
2014
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
2014
Titel
Overexpression of Bcl-3 inhibits the development of marginal zone B cells.
Sub types
  • Journal Article
  • Research Support, Non-U.S. Gov't
Ausgabe der Zeitschrift
44

Datenquelle: PubMed

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