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The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Cytosol-to-membrane redistribution of Bax and Bcl-XLduring apoptosis

Open access
Hsu, Yi-Te, Wolter, Keith G., Youle, Richard J.·1997·Proceedings of the National Academy of Sciences

Abstract

Bcl-2, Bcl-X L, and Bax are members of the Bcl-2 family that play key roles in the regulation of apoptosis. These proteins are believed to be membrane bound and their ability to undergo both homodimerization and heterodimerization has been proposed to regulate apoptosis. Herein we report that in murine thymocytes, Bcl-2 is exclusively membrane-bound, whereas Bax is present predominantly in the cytosol and Bcl-X L is present in both soluble and membrane-bound forms. Induction of apoptosis in murine thymocytes by dexamethasone or γ-irradiation shifts the subcellular locations of Bax and Bcl-X L from soluble to membrane-bound forms. A similar shift in the localization of Bax from the cytosol to membranes was observed in HL-60 leukemia cells upon induction of apoptosis by staurosporine. Inhibition of apoptosis with cycloheximide inhibits the movement of Bax and Bcl-X L in thymocytes from the cytosol into membranes induced by dexamethasone treatment. These movements may represent an important step in the pathway by which members of this family regulate apoptosis.

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Metadata

Authors
Hsu, Y.-T., Wolter, K. G., & Youle, R. J.
Venue
Proceedings of the National Academy of Sciences
Published
1997-04-15
Volume
94
Issue
8
Pages
3668-3672
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2033873142
Cited by
1,134
References
2
FWCI
18.11
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Cytosol-to-membrane redistribution of Bax and Bcl-XLduring apoptosis. https://app.cochat.ai/papers/10.1073/pnas.94.8.3668
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Hsu, Y.-T., Wolter, K. G., & Youle, R. J. (1997). Cytosol-to-membrane redistribution of Bax and Bcl-XLduring apoptosis. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.94.8.3668

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