The DOI matches its Crossref record; 80 of the 80 references it cites were found in a registry or an index.
AMPK and cell proliferation – AMPK as a therapeutic target for atherosclerosis and cancer
Open accessAbstract
AMPK is a serine/threonine protein kinase, which serves as an energy sensor in all eukaryotic cell types. Published studies indicate that AMPK activation strongly suppresses cell proliferation in non‐malignant cells as well as in tumour cells. These actions of AMPK appear to be mediated through multiple mechanisms including regulation of the cell cycle and inhibition of protein synthesis, de novo fatty acid synthesis, specifically the generation of mevalonate as well as other products downstream of mevalonate in the cholesterol synthesis pathway. Cell cycle regulation by AMPK is mediated by up‐regulation of the p53–p21 axis as well as regulation of TSC2–mTOR (mammalian target of rapamycin) pathway. The AMPK signalling network contains a number of tumour suppressor genes including LKB1, p53, TSC1 and TSC2, and overcomes growth factor signalling from a variety of stimuli (via growth factors and by abnormal regulation of cellular proto‐oncogenes including PI3K, Akt and ERK). These observations suggest that AMPK activation is a logical therapeutic target for diseases rooted in cellular proliferation, including atherosclerosis and cancer. In this review, we discuss about exciting recent advances indicating that AMPK functions as a suppressor of cell proliferation by controlling a variety of cellular events in normal cells as well as in tumour cells.
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
Role of AMP-Activated Protein Kinase in Mechanism of Metformin Action
Zhou, G., Myers, R., Li, Y., Chen, Y., Shen, X., Fenyk-Melody, J., Wu, M., Ventre, J., Doebber, T., Fujii, N., et al. (2001) · Journal of Clinical Investigation · doi:10.1172/jci13505 · Cited by 5,652
The phosphoinositide 3-kinase pathway
Cantley, L. C. (2002) · Science · doi:10.1126/science.296.5573.1655 · Cited by 5,621
Sherr, C. J. (1996) · Science · doi:10.1126/science.274.5293.1672 · Cited by 5,379
The retinoblastoma protein and cell cycle control
Weinberg, R. A. (1995) · Cell · doi:10.1016/0092-8674(95)90385-2 · Cited by 4,862
Yamauchi, T., Kamon, J., Minokoshi, Y., Ito, Y., Waki, H., Uchida, S., Yamashita, S., Noda, M., Kita, S., Ueki, K., et al. (2002) · Nature Medicine · doi:10.1038/nm788 · Cited by 4,238
TSC2 Mediates Cellular Energy Response to Control Cell Growth and Survival
Inoki, K., Zhu, T., & Guan, K.-L. (2003) · Cell · doi:10.1016/s0092-8674(03)00929-2 · Cited by 3,914
TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling
Inoki, K., Li, Y., Zhu, T., Wu, J., & Guan, K.-L. (2002) · Nature Cell Biology · doi:10.1038/ncb839 · Cited by 3,083
Metformin and reduced risk of cancer in diabetic patients
Evans, J. M. M., Donnelly, L. A., Emslie-Smith, A. M., Alessi, D. R., & Morris, A. D. (2005) · BMJ · doi:10.1136/bmj.38415.708634.f7 · Cited by 2,388
DNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2
Shieh, S.-Y., Ikeda, M., Taya, Y., & Prives, C. (1997) · Cell · doi:10.1016/s0092-8674(00)80416-x · Cited by 2,100
Cyclins and cancer II: Cyclin D and CDK inhibitors come of age
Hunter, T., & Pines, J. (1994) · Cell · doi:10.1016/0092-8674(94)90543-6 · Cited by 2,091
Cited by
p53 Target Genes Sestrin1 and Sestrin2 Connect Genotoxic Stress and mTOR Signaling
Budanov, A. V., & Karin, M. (2008) · Cell · doi:10.1016/j.cell.2008.06.028 · Cited by 1,326
Regulation of Immune Responses by mTOR
Powell, J. D., Pollizzi, K. N., Heikamp, E. B., & Horton, M. R. (2012) · Annual Review of Immunology · doi:10.1146/annurev-immunol-020711-075024 · Cited by 836
Resveratrol stimulates AMP kinase activity in neurons
Dasgupta, B., & Milbrandt, J. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0610068104 · Cited by 723
Alimova, I. N., Liu, B., Fan, Z., Edgerton, S. M., Dillon, T., Lind, S. E., & Thor, A. D. (2009) · Cell Cycle · doi:10.4161/cc.8.6.7933 · Cited by 523
AMP-Activated Protein Kinase in the Heart: Role During Health and Disease
Arad, M., Seidman, C. E., & Seidman, J. G. (2007) · Circulation Research · doi:10.1161/01.res.0000258446.23525.37 · Cited by 362
Zheng, B., Jeong, J. H., Asara, J. M., Yuan, Y.-Y., Granter, S. R., Chin, L., & Cantley, L. C. (2009) · Molecular Cell · doi:10.1016/j.molcel.2008.12.026 · Cited by 359
Song, J., He, Y., Luo, C., Feng, B., Ran, F., Xu, H., Ci, Z., Xu, R., Han, L., & Zhang, D. (2020) · Pharmacological Research · doi:10.1016/j.phrs.2020.105109 · Cited by 303
DNA replication stress, genome instability and aging
Burhans, W. C., & Weinberger, M. (2007) · Nucleic Acids Research · doi:10.1093/nar/gkm1059 · Cited by 279
Cardioprotection by resveratrol: a novel mechanism via autophagy involving the mTORC2 pathway
Gurusamy, N., Lekli, I., Mukherjee, S., Ray, D., Ahsan, M. K., Gherghiceanu, M., Popescu, L. M., & Das, D. K. (2010) · Cardiovascular Research · doi:10.1093/cvr/cvp384 · Cited by 263
Marin, T. L., Gongol, B., Zhang, F., Martin, M., Johnson, D. A., Xiao, H., Wang, Y., Subramaniam, S., Chien, S., & Shyy, J. Y.-J. (2017) · Science Signaling · doi:10.1126/scisignal.aaf7478 · Cited by 257
Metformin suppresses intestinal polyp growth in Apc Min/+ mice
Tomimoto, A., Endo, H., Sugiyama, M., Fujisawa, T., Hosono, K., Takahashi, H., Nakajima, N., Nagashima, Y., Wada, K., Nakagama, H., et al. (2008) · Cancer Science · doi:10.1111/j.1349-7006.2008.00933.x · Cited by 185
Yoon, J. Y., Kwon, H. H., Min, S. U., Thiboutot, D. M., & Suh, D. H. (2013) · Journal of Investigative Dermatology · doi:10.1038/jid.2012.292 · Cited by 183
Hao, W., Chang, C.-P. B., Tsao, C.-C., & Xu, J. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.084194 · Cited by 138
Paranjpe, S., Bowen, W. C., Mars, W. M., Orr, A., Haynes, M. M., DeFrances, M. C., Liu, S., Tseng, G. C., Tsagianni, A., & Michalopoulos, G. K. (2016) · Hepatology · doi:10.1002/hep.28721 · Cited by 115
Zordoky, B. N. M., Bark, D., Soltys, C. L., Sung, M. M., & Dyck, J. R. B. (2014) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2014.01.023 · Cited by 98
Hyperglycemia Alters Astrocyte Metabolism and Inhibits Astrocyte Proliferation
Li, W., Roy Choudhury, G., Winters, A., Prah, J., Lin, W., Liu, R., & Yang, S.-H. (2018) · Aging and disease · doi:10.14336/ad.2017.1208 · Cited by 92
Tuo, L., Xiang, J., Pan, X., Hu, J., Tang, H., Liang, L., Xia, J., Hu, Y., Zhang, W., Huang, A., et al. (2019) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-019-1029-y · Cited by 84
Zhang, M., Dong, Y., Xu, J., Xie, Z., Wu, Y., Song, P., Guzman, M., Wu, J., & Zou, M.-H. (2008) · Circulation Research · doi:10.1161/circresaha.107.163253 · Cited by 82
AMP-activated protein kinase conducts the ischemic stress response orchestra
Young, L. H. (2008) · Circulation · doi:10.1161/circulationaha.107.713115 · Cited by 82
Blandino-Rosano, M., Perez-Arana, G., Mellado-Gil, J. M., Segundo, C., & Aguilar-Diosdado, M. (2008) · Journal of Molecular Endocrinology · doi:10.1677/jme-07-0154 · Cited by 82
Moeinabadi-Bidgoli, K., Babajani, A., Yazdanpanah, G., Farhadihosseinabadi, B., Jamshidi, E., Bahrami, S., & Niknejad, H. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.112026 · Cited by 70
Shimanuki, M., Chung, S., Chikashige, Y., Kawasaki, Y., Uehara, L., Tsutsumi, C., Hatanaka, M., Hiraoka, Y., Nagao, K., & Yanagida, M. (2007) · Genes to Cells · doi:10.1111/j.1365-2443.2007.01079.x · Cited by 62
Ha, S., Jeong, S.-H., Yi, K., Chung, K. M., Hong, C. J., Kim, S. W., Kim, E.-K., & Yu, S.-W. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m117.780874 · Cited by 61
Candidate mechanisms accounting for effects of physical activity on breast carcinogenesis
Thompson, H. J., Jiang, W., & Zhu, Z. (2009) · IUBMB Life · doi:10.1002/iub.233 · Cited by 59
“mTOR is centrally involved in cell growth, that is, increase in cell size and cell mass, and these processes are tightly coupled to cell division (reviewed in (15)).”
Background(2010) · PubMed Central · Cited by 46
Connolly, K., Mitter, R., Muir, M., Jodrell, D., & Guichard, S. (2009) · Cancer Chemotherapy and Pharmacology · doi:10.1007/s00280-008-0872-x · Cited by 34
Metadata
- Authors
- Motoshima, H., Goldstein, B. J., Igata, M., & Araki, E.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2006-06-19
- Volume
- 574
- Issue
- 1
- Pages
- 63-71
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- OpenAlex
- W1563676220
- Cited by
- 527
- References
- 80
- FWCI
- 12.16
- 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
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.
