PMID: 15240668Jul 9, 2004Paper

Decreased E47 in senescent B cell precursors is stage specific and regulated posttranslationally by protein turnover

The Journal of Immunology : Official Journal of the American Association of Immunologists
Elaine Van der PutRichard L Riley

Abstract

The E2A-encoded transcription factor E47 is crucial to B lymphopoiesis. Senescent BALB/c mice ( approximately 2 years old) had reduced pre-B cells ex vivo. Pro-B/early pre-B cells from these aged mice, both ex vivo and in vitro, were deficient in E47 protein. In vitro, IL-7 expanded pro-B/early pre-B cells from young BALB/c mice expressed E47 protein that was relatively stable over a 5-h period. Cultured senescent pro-B/early pre-B cells exhibited reduced E47 protein stability with approximately 50-90% loss of E47 over the same time period. Degradation of E47 was effectively blocked by the proteasome inhibitor lactacystin as well as calpain I and II inhibitors; E2A proteins were also shown to undergo ubiquitination. Although senescent B cell precursors expressed less E47 protein, E47 mRNA levels and turnover were normal. Therefore, E47 protein levels are reduced relatively early in B lineage differentiation in senescence and the decline in E47 protein occurs via increased protein degradation by proteasome and, possibly, calpain pathways. In contrast, normal E47 protein levels were observed within the highly reduced pre-B cell pool in aged mice. This suggests that pre-B cells in senescence undergo selection based on E47 expressi...Continue Reading

References

May 1, 1991·The Journal of Experimental Medicine·R R HardyK Hayakawa
Feb 1, 1991·Molecular and Cellular Biology·C MurreD Baltimore
Nov 1, 1994·Trends in Pharmacological Sciences·K K Wang, P W Yuen
Jun 21, 1994·Biochimica Et Biophysica Acta·C MurreM H Stuiver
Apr 1, 1996·International Immunology·R P StephanP L Witte
Dec 1, 1996·Molecular and Cellular Biology·S R SloanT Kadesch
Feb 7, 1997·The Journal of Biological Chemistry·C J KhoE Haber
Nov 14, 1997·The Journal of Biological Chemistry·Y H ChoiJ B Trepel
Feb 26, 1998·Immunological Reviews·N R Klinman, G H Kline
Jun 10, 1998·Seminars in Immunology·G Bain, C Murre
Jun 30, 1998·European Journal of Immunology·L LuD G Osmond
Sep 25, 1999·The Journal of Biological Chemistry·G S HugginsM E Lee
Dec 15, 2000·The Journal of Biological Chemistry·C Chu, D S Kohtz
Jan 11, 2002·Molecular and Cellular Biology·Sabine HerblotTrang Hoang
Feb 28, 2002·Annual Review of Immunology·Melanie W QuongCornelis Murre
Jul 20, 2002·The International Journal of Biochemistry & Cell Biology·Belinda J WestmanDavid Gell
Jan 9, 2003·The Journal of Immunology : Official Journal of the American Association of Immunologists·Daniela FrascaBonnie B Blomberg
Mar 14, 2003·Current Opinion in Immunology·Richard R Hardy
Apr 30, 2003·Nature Immunology·Camil Elie SayeghCornelis Murre
Jun 12, 2003·Cellular Immunology·Paul SzaboMarc E Weksler
Oct 29, 2003·Experimental Gerontology·Elaine Van der PutRichard L Riley
Feb 7, 2004·The Journal of Immunology : Official Journal of the American Association of Immunologists·Daniela FrascaBonnie B Blomberg

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Citations

Jul 22, 2015·Annals of the New York Academy of Sciences·Nichol E Holodick, Thomas L Rothstein
Nov 30, 2016·Frontiers in Immunology·Larisa V KovtonyukHitoshi Takizawa
Jan 6, 2006·The Journal of Immunology : Official Journal of the American Association of Immunologists·Hyeyoung MinKenneth Dorshkind
May 11, 2005·Immunological Reviews·David Allman, Juli P Miller
Sep 27, 2008·Immunologic Research·Daniel L Northrup, David Allman
Feb 23, 2007·Immunology·Danielle AwDonald B Palmer
Jan 19, 2011·Aging Cell·Ana M LandinBonnie B Blomberg
Jul 5, 2013·The Journal of Immunology : Official Journal of the American Association of Immunologists·Kristin JensenKaare M Gautvik
May 11, 2005·Immunological Reviews·Hyeyoung MinKenneth Dorshkind
Nov 8, 2005·The Journal of Immunology : Official Journal of the American Association of Immunologists·Daniela FrascaBonnie B Blomberg
Dec 26, 2008·The Journal of Immunology : Official Journal of the American Association of Immunologists·Sarah Alter-WolfRichard L Riley
Sep 24, 2009·Immunology and Cell Biology·Daisuke HidaKen-Ichi Isobe
Mar 29, 2011·The Journal of Immunology : Official Journal of the American Association of Immunologists·Brandt L EsplinPaul W Kincade
May 11, 2005·Immunological Reviews·Richard L RileyDaniela Frasca
Mar 7, 2007·The Journal of Immunology : Official Journal of the American Association of Immunologists·Anne M KingRichard L Riley
Oct 22, 2005·Nature Immunology·Cornelis Murre
Nov 10, 2013·Immunologic Research·Richard L Riley
Nov 26, 2011·The Journal of Immunology : Official Journal of the American Association of Immunologists·Daniela FrascaBonnie B Blomberg
Feb 23, 2008·The Journal of Immunology : Official Journal of the American Association of Immunologists·Daniela FrascaBonnie B Blomberg
Nov 10, 2013·Immunologic Research·Bonnie B Blomberg, Daniela Frasca
Feb 9, 2021·Cytokine & Growth Factor Reviews·Leane Perim RodriguesJuliana Lott Carvalho
Jul 18, 2009·Current Opinion in Immunology·Daniela Frasca, Bonnie B Blomberg
Jun 7, 2020·Experimental Gerontology·Verena Labi, Emmanuel Derudder
Apr 4, 2021·Cell·Jaime L SchneiderMarcia C Haigis
Jun 20, 2006·Immunity·Encarnacion Montecino-Rodriguez, Kenneth Dorshkind
Jun 28, 2005·Seminars in Immunology·Juli P Miller, David Allman
Aug 19, 2021·Best Practice & Research. Clinical Haematology·Janice ZhaoJane Liesveld

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