The DOI matches its OpenAlex record; 8 of the 8 references it cites were found in a registry or an index.
Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury.
Open accessAbstract
Protein kinase B, also known as Akt, is a serine/threonine kinase and plays a critical role in the modulation of cell development, growth, and survival. Interestingly, Akt is ubiquitously expressed throughout the body, but its expression in the nervous system is substantially up-regulated during cellular stress, suggesting a more expansive role for Akt in the nervous system that may involve cellular protection. In this regard, a body of recent work has identified a robust capacity for Akt and its downstream substrates to foster both neuronal and vascular survival during apoptotic injury. Cell survival by Akt is driven by the modulation of both intrinsic cellular pathways that oversee genomic DNA integrity and extrinsic mechanisms that control inflammatory microglial activation. A series of distinct pathways are regulated by Akt that include the Forkhead family of transcription factors, GSK-3 beta, beta-catenin, c-Jun, CREB, Bad, IKK, and p53. Culminating below these substrates of Akt are the control of caspase mediated pathways that promote genomic integrity as well as prevent inflammatory cell demise. With further levels of progress in defining the cellular role of Akt, the attractiveness of Akt as a vital and broad cytoprotectant for both neuronal and vascular cell populations should continue to escalate.
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
Death Receptors: Signaling and Modulation
Ashkenazi, A., & Dixit, V. M. (1998) · Science · doi:10.1126/science.281.5381.1305 · Cited by 5,866
Stress-dependent regulation of FOXO transcription factors by the SIRT1 deacetylase
Brunet, A., Sweeney, L. B., Sturgill, J. F., Chua, K. F., Greer, P. L., Lin, Y., Tran, H., Ross, S. E., Mostoslavsky, R., Cohen, H. Y., et al. (2004) · Science · doi:10.1126/science.1094637 · Cited by 3,239
Forkhead transcription factor FOXO3a protects quiescent cells from oxidative stress
Kops, G. J. P. L., Dansen, T. B., Polderman, P. E., Saarloos, I., Wirtz, K. W. A., Coffer, P. J., Huang, T.-T., Bos, J. L., Medema, R. H., & Burgering, B. M. T. (2002) · Nature · doi:10.1038/nature01036 · Cited by 1,580
Induction of gadd45β by NF-κB downregulates pro-apoptotic JNK signalling
De Smaele, E., Zazzeroni, F., Papa, S., Nguyen, D. U., Jin, R., Jones, J., Cong, R., & Franzoso, G. (2001) · Nature · doi:10.1038/35104560 · Cited by 732
Yamamoto, H., Kishida, S., Kishida, M., Ikeda, S., Takada, S., & Kikuchi, A. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.16.10681 · Cited by 364
Frödin, M., Antal, T. L., Dümmler, B. A., Jensen, C. J., Deak, M., Gammeltoft, S., & Biondi, R. M. (2002) · The EMBO Journal · doi:10.1093/emboj/cdf551 · Cited by 275
Yamaguchi, A., Tamatani, M., Matsuzaki, H., Namikawa, K., Kiyama, H., Vitek, M. P., Mitsuda, N., & Tohyama, M. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m008552200 · Cited by 242
Requirement of the JIP1 scaffold protein for stress-induced JNK activation
Whitmarsh, A. J., Kuan, C.-Y., Kennedy, N. J., Kelkar, N., Haydar, T. F., Mordes, J. P., Appel, M., Rossini, A. A., Jones, S. N., Flavell, R. A., et al. (2001) · Genes & Development · doi:10.1101/gad.922801 · Cited by 238
Cited by
The chemical biology of nitric oxide: Implications in cellular signaling
Thomas, D. D., Ridnour, L. A., Isenberg, J. S., Flores-Santana, W., Switzer, C. H., Donzelli, S., Hussain, P., Vecoli, C., Paolocci, N., Ambs, S., et al. (2008) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2008.03.020 · Cited by 975
Chong, Z. Z., Li, F., & Maiese, K. (2005) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2005.02.004 · Cited by 536
Self-citationNitric oxide release: Part III. Measurement and reporting
Coneski, P. N., & Schoenfisch, M. H. (2012) · Chemical Society Reviews · doi:10.1039/c2cs15271a · Cited by 360
OutFOXOing disease and disability: the therapeutic potential of targeting FoxO proteins
Maiese, K., Chong, Z. Z., & Shang, Y. C. (2008) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2008.03.002 · Cited by 182
Self-citationShedding new light on neurodegenerative diseases through the mammalian target of rapamycin
Chong, Z. Z., Shang, Y. C., Wang, S., & Maiese, K. (2012) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2012.08.001 · Cited by 119
Self-citation
Metadata
- Authors
- Chong, Z. Z., Li, F., & Maiese, K.
- Venue
- PubMed
- Publisher
- National Institutes of Health
- Published
- 2005-01-01
- Volume
- 20
- Issue
- 1
- Pages
- 299-315
- OpenAlex
- W2112237379
- Cited by
- 182
- References
- 8
- FWCI
- 5.42
- 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: Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. https://app.cochat.ai/papers/10.14670/hh-20.299
- The paper
- Chong, Z. Z., Li, F., & Maiese, K. (2005). Activating Akt and the brain's resources to drive cellular survival and prevent inflammatory injury. PubMed. https://doi.org/10.14670/hh-20.299
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.
