The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Cytokine-mediated Bax deficiency and consequent delayed neutrophil apoptosis: A general mechanism to accumulate effector cells in inflammation
Open accessAbstract
Neutrophils are important effector cells in immunity to microorganisms, particularly bacteria. Here, we show that the process of neutrophil apoptosis is delayed in several inflammatory diseases, suggesting that this phenomenon may represent a general feature contributing to the development of neutrophilia, and, therefore, in many cases to host defense against infection. The delay of neutrophil apoptosis was associated with markedly reduced levels of Bax, a pro-apoptotic member of the Bcl-2 family. Such Bax-deficient cells were also observed upon stimulation of normal neutrophils with cytokines present at sites of neutrophilic inflammation, such as granulocyte and granulocyte–macrophage colony-stimulating factors, in vitro . Moreover, Bax-deficient neutrophils generated by using Bax antisense oligodeoxynucleotides demonstrated delayed apoptosis, providing direct evidence for a role of Bax as a pro-apoptotic molecule in these cells. Interestingly, the Bax gene was reexpressed in Bax-deficient neutrophils under conditions of cytokine withdrawal. Thus, both granulocyte expansion and the resolution of inflammation appear to be regulated by the expression of the Bax gene in neutrophils.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
Oltval, Z. N., Milliman, C. L., & Korsmeyer, S. J. (1993) · Cell · doi:10.1016/0092-8674(93)90509-o · Cited by 6,003
Shimizu, S., Narita, M., Tsujimoto, Y., & Tsujimoto, Y. (1999) · Nature · doi:10.1038/20959 · Cited by 2,178
Savill, J. S., Wyllie, A. H., Henson, J. E., Walport, M. J., Henson, P. M., & Haslett, C. (1989) · Journal of Clinical Investigation · doi:10.1172/jci113970 · Cited by 1,536
Bax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of Apoptosis
Marzo, I., Brenner, C., Zamzami, N., Jürgensmeier, J. M., Susin, S. A., Vieira, H. L. A., Prévost, M.-C., Xie, Z., Matsuyama, S., Reed, J. C., et al. (1998) · Science · doi:10.1126/science.281.5385.2027 · Cited by 1,168
Martich, G. D., Danner, R. L., Ceska, M., & Suffredini, A. F. (1991) · The Journal of Experimental Medicine · doi:10.1084/jem.173.4.1021 · Cited by 444
Cited by
Role of reactive oxygen species (ROS) in apoptosis induction
Simon, H.-U., Haj-Yehia, A., & Levi-Schaffer, F. (2000) · Apoptosis · doi:10.1023/a:1009616228304 · Cited by 2,774
Self-citationMcLoughlin, R. M., Witowski, J., Robson, R. L., Wilkinson, T. S., Hurst, S. M., Williams, A. S., Williams, J. D., Rose-John, S., Jones, S. A., & Topley, N. (2003) · Journal of Clinical Investigation · doi:10.1172/jci17129 · Cited by 281
Living and dying for inflammation: neutrophils, eosinophils, basophils
Geering, B., Stoeckle, C., Conus, S., & Simon, H.-U. (2013) · Trends in Immunology · doi:10.1016/j.it.2013.04.002 · Cited by 256
Self-citationTehranchi, R. (2005) · Blood · doi:10.1182/blood-2004-12-4649 · Cited by 104
In Vivo Interleukin-6 Protects Neutrophils from Apoptosis in Osteomyelitis
Asensi, V., Valle, E., Meana, A., Fierer, J., Celada, A., Alvarez, V., Paz, J., Coto, E., Carton, J. A., Maradona, J. A., et al. (2004) · Infection and Immunity · doi:10.1128/iai.72.7.3823-3828.2004 · Cited by 93
Metadata
- Authors
- Dibbert, B., Weber, M., Nikolaizik, W. H., Vogt, P., Schöni, M. H., Blaser, K., & Simon, H.-U.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-11-09
- Volume
- 96
- Issue
- 23
- Pages
- 13330-13335
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1976968664
- Cited by
- 278
- References
- 5
- FWCI
- 5.44
- Type
- journal article
- Language
- en
- Open access
- green
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Cytokine-mediated Bax deficiency and consequent delayed neutrophil apoptosis: A general mechanism to accumulate effector cells in inflammation. https://app.cochat.ai/papers/10.1073/pnas.96.23.13330
- The paper
- Dibbert, B., Weber, M., Nikolaizik, W. H., Vogt, P., Schöni, M. H., Blaser, K., & Simon, H.-U. (1999). Cytokine-mediated Bax deficiency and consequent delayed neutrophil apoptosis: A general mechanism to accumulate effector cells in inflammation. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.23.13330
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
