The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Overexpression of thioredoxin in transgenic mice attenuates focal ischemic brain damage
Open accessAbstract
Thioredoxin (TRX) plays important biological roles both in intra- and extracellular compartments, including in regulation of various intracellular molecules via thiol redox control. We produced TRX overexpressing mice and confirmed that there were no anatomical and physiological differences between wild-type (WT) mice and TRX transgenic (Tg) mice. In the present study we subjected mice to focal brain ischemia to shed light on the role of TRX in brain ischemic injury. At 24 hr after middle cerebral artery occlusion, infarct areas and volume were significantly smaller in Tg mice than in WT mice. Moreover neurological deficit was ameliorated in Tg mice compared with WT mice. Protein carbonyl content, a marker of cellular protein oxidation, in Tg mice showed less increase than did that of WT mice after the ischemic insult. Furthermore, c-fos expression in Tg mice was stronger than in WT mice 1 hr after ischemia. Our results suggest that transgene expression of TRX decreased ischemic neuronal injury and that TRX and the redox state modified by TRX play a crucial role in brain damage during stroke.
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
Reversible middle cerebral artery occlusion without craniectomy in rats.
Longa, E. Z., Weinstein, P. R., Carlson, S., & Cummins, R. (1989) · Stroke · doi:10.1161/01.str.20.1.84 · Cited by 7,463
Mammalian thioredoxin is a direct inhibitor of apoptosis signal‐regulating kinase (ASK) 1
Saitoh, M., Nishitoh, H., Fujii, M., Takeda, K., Tobiume, K., Sawada, Y., Kawabata, M., Miyazono, K., & Ichijo, H. (1998) · The EMBO Journal · doi:10.1093/emboj/17.9.2596 · Cited by 2,377
Redox Regulation of Fos and Jun DNA-Binding Activity in Vitro
Abate, C., Patel, L., Rauscher, F. J., & Curran, T. (1990) · Science · doi:10.1126/science.2118682 · Cited by 1,573
Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease.
Smith, C. D., Carney, J. M., Starke-Reed, P. E., Oliver, C. N., Stadtman, E. R., Floyd, R. A., & Markesbery, W. R. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.23.10540 · Cited by 1,296
Cited by
Halliwell, B. (2001) · Drugs & Aging · doi:10.2165/00002512-200118090-00004 · Cited by 1,502
Hydrogen peroxide in the human body
Halliwell, B., Clement, M. V., & Long, L. H. (2000) · FEBS Letters · doi:10.1016/s0014-5793(00)02197-9 · Cited by 1,075
Trends in oxidative aging theories
Muller, F. L., Lustgarten, M. S., Jang, Y., Richardson, A., & Van Remmen, H. (2007) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2007.03.034 · Cited by 1,053
Thioredoxin and Related Molecules–From Biology to Health and Disease
Lillig, C. H., & Holmgren, A. (2007) · Antioxidants & Redox Signaling · doi:10.1089/ars.2007.9.25 · Cited by 724
Hanschmann, E.-M., Godoy, J. R., Berndt, C., Hudemann, C., & Lillig, C. H. (2013) · Antioxidants & Redox Signaling · doi:10.1089/ars.2012.4599 · Cited by 677
Metadata
- Authors
- Takagi, Y., Mitsui, A., Nishiyama, A., Nozaki, K., Sono, H., Gon, Y., Hashimoto, N., & Yodoi, J.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-03-30
- Volume
- 96
- Issue
- 7
- Pages
- 4131-4136
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2026512497
- Cited by
- 336
- References
- 4
- FWCI
- 6.74
- 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: Overexpression of thioredoxin in transgenic mice attenuates focal ischemic brain damage. https://app.cochat.ai/papers/10.1073/pnas.96.7.4131
- The paper
- Takagi, Y., Mitsui, A., Nishiyama, A., Nozaki, K., Sono, H., Gon, Y., Hashimoto, N., & Yodoi, J. (1999). Overexpression of thioredoxin in transgenic mice attenuates focal ischemic brain damage. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.7.4131
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.