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Article: Developmental regulation of apoptosis and BCL-2/BAX expression during B lymphopoiesis in normal and RAG-2-/- mouse bone marrow

TitleDevelopmental regulation of apoptosis and BCL-2/BAX expression during B lymphopoiesis in normal and RAG-2-/- mouse bone marrow
Authors
Issue Date1998
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 1998, v. 12 n. 5, p. A1080 How to Cite?
AbstractB cell genesis in mouse bone marrow (BM) represents a finely controlled balance between cell production and apoptotic cell selection. However, the molecular signals that modulate B cell selection in BM are unclear. In the present study, we have examined Bcl-2 and Bax protein expression among precursor B cells at phenotypically defined differentiation stages in normal mouse BM cell suspensions using Western blotting and flow cytometry. The mean concentration of Bcl-2 and Bax per cell changed during successive stages of B cell development, high Bax/Bcl-2 ratios generally correlating with high incidences of hypodiploid apoptotic cells detected by flow cytometry among large pre-B cells and immature B lymphocytes, respectively. Further, the B220+μ- early precursor B cells in RAG-2-/- mouse BM showed a high apoptotic incidence ex vivo and an accelerated rate of entry into the apoptotic pathway in short term culture, together with an elevated Bax/Bcl-2 protein ratio. Changes in Bax/Bcl-2 ratio, similarly correlated with modified apoptotic rates among precursor B cells, were also observed in interleukin-7 gene modified mice. These findings suggest that Bcl-2 family proteins are implicated in regulating apoptotic selection of precursor B cells during their development in mouse BM.
Persistent Identifierhttp://hdl.handle.net/10722/148481
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorOsmond, DGen_US
dc.contributor.authorLu, Len_US
dc.date.accessioned2012-05-29T06:13:12Z-
dc.date.available2012-05-29T06:13:12Z-
dc.date.issued1998en_US
dc.identifier.citationFaseb Journal, 1998, v. 12 n. 5, p. A1080en_US
dc.identifier.issn0892-6638en_US
dc.identifier.urihttp://hdl.handle.net/10722/148481-
dc.description.abstractB cell genesis in mouse bone marrow (BM) represents a finely controlled balance between cell production and apoptotic cell selection. However, the molecular signals that modulate B cell selection in BM are unclear. In the present study, we have examined Bcl-2 and Bax protein expression among precursor B cells at phenotypically defined differentiation stages in normal mouse BM cell suspensions using Western blotting and flow cytometry. The mean concentration of Bcl-2 and Bax per cell changed during successive stages of B cell development, high Bax/Bcl-2 ratios generally correlating with high incidences of hypodiploid apoptotic cells detected by flow cytometry among large pre-B cells and immature B lymphocytes, respectively. Further, the B220+μ- early precursor B cells in RAG-2-/- mouse BM showed a high apoptotic incidence ex vivo and an accelerated rate of entry into the apoptotic pathway in short term culture, together with an elevated Bax/Bcl-2 protein ratio. Changes in Bax/Bcl-2 ratio, similarly correlated with modified apoptotic rates among precursor B cells, were also observed in interleukin-7 gene modified mice. These findings suggest that Bcl-2 family proteins are implicated in regulating apoptotic selection of precursor B cells during their development in mouse BM.en_US
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_US
dc.relation.ispartofFASEB Journalen_US
dc.titleDevelopmental regulation of apoptosis and BCL-2/BAX expression during B lymphopoiesis in normal and RAG-2-/- mouse bone marrowen_US
dc.typeArticleen_US
dc.identifier.emailLu, L:liweilu@hkucc.hku.hken_US
dc.identifier.authorityLu, L=rp00477en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-33749364038en_US
dc.identifier.volume12en_US
dc.identifier.issue5en_US
dc.identifier.spageA1080en_US
dc.publisher.placeUnited Statesen_US

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