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Cited by 395

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Bcl-XL and Bcl-2 repress a common pathway of cell death.

Open access
Chao, D T, Linette, G P, Boise, L H, White, L S, Thompson, C B, Korsmeyer, S J·1995·The Journal of experimental medicine

Abstract

The effect of Bcl-xL upon the developmental death of T cells was assessed by generating transgenic mice that expressed Bcl-xL within all thymocyte subsets. Bcl-xL protected thymocytes from a variety of apoptotic stimuli, including gamma irradiation, glucocorticoids, and anti-CD3 treatment. Bcl-xL altered thymocyte maturation, resulting in increased numbers of CD3int/hi and CD4-8+ thymocytes. Overall, the phenotype of Bcl-xL transgenics was essentially indistinguishable from a Bcl-2 transgenic model. Overexpression of Bcl-xL or Bcl-2 resulted in the down-regulation of the other molecule, providing further evidence of their reciprocal regulation. In a genetic test of redundancy, the Bcl-xL transgene rescued mature T cells in Bcl-2 null mice. Immunoprecipitation indicated that Bcl-xL, like Bcl-2, heterodimerized with the death-promoting molecule Bax in thymocytes. This in vivo model argues that Bcl-xL, like Bcl-2, functions in a common pathway to repress cell death.

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Metadata

Authors
Chao, D. T., Linette, G. P., Boise, L. H., White, L. S., Thompson, C. B., & Korsmeyer, S. J.
Venue
The Journal of experimental medicine
Published
1995-09-01
Volume
182
Issue
3
Pages
821-828
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2131616553
Cited by
395
References
1
FWCI
10.30
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Bcl-XL and Bcl-2 repress a common pathway of cell death. https://app.cochat.ai/papers/10.1084/jem.182.3.821
The paper
Chao, D. T., Linette, G. P., Boise, L. H., White, L. S., Thompson, C. B., & Korsmeyer, S. J. (1995). Bcl-XL and Bcl-2 repress a common pathway of cell death. The Journal of experimental medicine. https://doi.org/10.1084/jem.182.3.821

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.