File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1002/(SICI)1521-4141(199908)29:08<2484::AID-IMMU2484>3.0.CO;2-B
- Scopus: eid_2-s2.0-0032773042
- PMID: 10458762
- WOS: WOS:000082042500015
- Find via
Supplementary
- Citations:
- Appears in Collections:
Article: Regulation of cell survival during B lymphopoiesis: Suppressed apoptosis of pro-B cells in P53-deficient mouse bone marrow
Title | Regulation of cell survival during B lymphopoiesis: Suppressed apoptosis of pro-B cells in P53-deficient mouse bone marrow |
---|---|
Authors | |
Keywords | Apoptosis B lymphocyte Bone marrow P53 gene |
Issue Date | 1999 |
Publisher | Wiley - V C H Verlag GmbH & Co KGaA. The Journal's web site is located at http://www.eji.de |
Citation | European Journal Of Immunology, 1999, v. 29 n. 8, p. 2484-2490 How to Cite? |
Abstract | B cell development in mouse bone marrow (BM) is subject to quality controls that eliminate aberrant cells by apoptosis, but the intrinsic cellular mechanisms that mediate this negative B cell selection remain unclear. The p53 tumor suppressor transduces signals resulting in apoptosis and cell cycle arrest in cells that sustain DNA damage. Faulty V(D)J recombination in scid lymphocyte precursors activates a p53-dependent DNA damage checkpoint. In the present study, we have examined whether p53 is involved in apoptotic selection of normally developing B cells in BM. Double immunofluorescence labeling and flow cytometry were used to quantitate phenotypically defined B cell populations and their apoptotic rates in BM of homozygous p53-deficient mice. B220+ μ- and terminal deoxynucleotidyl transferase (TdT)+ pro-B cells were increased in both incidence and absolute number to controls. In contrast, pre-B cells were only slightly increased and the sIgM+ B lymphocyte compartment remained essentially normal. The incidence of apoptosis among p53(-/-) pro-B cells was greatly reduced, both ex vivo and in short-term culture, whereas, apoptosis of pre-B cells and B lymphocytes was not significantly different from normal. The results indicate that p53 is actively involved as an apoptosis inducer at an early quality control checkpoint in B lymphopoiesis. |
Persistent Identifier | http://hdl.handle.net/10722/148138 |
ISSN | 2023 Impact Factor: 4.5 2023 SCImago Journal Rankings: 1.627 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lu, L | en_US |
dc.contributor.author | Lejtenyi, D | en_US |
dc.contributor.author | Osmond, DG | en_US |
dc.date.accessioned | 2012-05-29T06:11:04Z | - |
dc.date.available | 2012-05-29T06:11:04Z | - |
dc.date.issued | 1999 | en_US |
dc.identifier.citation | European Journal Of Immunology, 1999, v. 29 n. 8, p. 2484-2490 | en_US |
dc.identifier.issn | 0014-2980 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/148138 | - |
dc.description.abstract | B cell development in mouse bone marrow (BM) is subject to quality controls that eliminate aberrant cells by apoptosis, but the intrinsic cellular mechanisms that mediate this negative B cell selection remain unclear. The p53 tumor suppressor transduces signals resulting in apoptosis and cell cycle arrest in cells that sustain DNA damage. Faulty V(D)J recombination in scid lymphocyte precursors activates a p53-dependent DNA damage checkpoint. In the present study, we have examined whether p53 is involved in apoptotic selection of normally developing B cells in BM. Double immunofluorescence labeling and flow cytometry were used to quantitate phenotypically defined B cell populations and their apoptotic rates in BM of homozygous p53-deficient mice. B220+ μ- and terminal deoxynucleotidyl transferase (TdT)+ pro-B cells were increased in both incidence and absolute number to controls. In contrast, pre-B cells were only slightly increased and the sIgM+ B lymphocyte compartment remained essentially normal. The incidence of apoptosis among p53(-/-) pro-B cells was greatly reduced, both ex vivo and in short-term culture, whereas, apoptosis of pre-B cells and B lymphocytes was not significantly different from normal. The results indicate that p53 is actively involved as an apoptosis inducer at an early quality control checkpoint in B lymphopoiesis. | en_US |
dc.language | eng | en_US |
dc.publisher | Wiley - V C H Verlag GmbH & Co KGaA. The Journal's web site is located at http://www.eji.de | en_US |
dc.relation.ispartof | European Journal of Immunology | en_US |
dc.subject | Apoptosis | - |
dc.subject | B lymphocyte | - |
dc.subject | Bone marrow | - |
dc.subject | P53 gene | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Apoptosis | en_US |
dc.subject.mesh | B-Lymphocytes - Cytology - Immunology - Metabolism | en_US |
dc.subject.mesh | Cell Differentiation | en_US |
dc.subject.mesh | Cell Survival | en_US |
dc.subject.mesh | Genes, P53 | en_US |
dc.subject.mesh | Hematopoietic Stem Cells - Cytology - Immunology - Metabolism | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mice, Knockout | en_US |
dc.subject.mesh | Tumor Suppressor Protein P53 - Deficiency - Genetics | en_US |
dc.title | Regulation of cell survival during B lymphopoiesis: Suppressed apoptosis of pro-B cells in P53-deficient mouse bone marrow | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lu, L:liweilu@hkucc.hku.hk | en_US |
dc.identifier.authority | Lu, L=rp00477 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1002/(SICI)1521-4141(199908)29:08<2484::AID-IMMU2484>3.0.CO;2-B | en_US |
dc.identifier.pmid | 10458762 | en_US |
dc.identifier.scopus | eid_2-s2.0-0032773042 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0032773042&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 29 | en_US |
dc.identifier.issue | 8 | en_US |
dc.identifier.spage | 2484 | en_US |
dc.identifier.epage | 2490 | en_US |
dc.identifier.isi | WOS:000082042500015 | - |
dc.publisher.place | Germany | en_US |
dc.identifier.issnl | 0014-2980 | - |