The DOI matches its Crossref record; 263 of the 263 references it cites were found in a registry or an index.
LPA receptor signaling: pharmacology, physiology, and pathophysiology
Open accessAbstract
Lysophosphatidic acid (LPA) is a small ubiquitous lipid found in vertebrate and nonvertebrate organisms that mediates diverse biological actions and demonstrates medicinal relevance. LPA's functional roles are driven by extracellular signaling through at least six 7-transmembrane G protein-coupled receptors. These receptors are named LPA1-6 and signal through numerous effector pathways activated by heterotrimeric G proteins, including Gi/o, G12/13, Gq, and Gs LPA receptor-mediated effects have been described in numerous cell types and model systems, both in vitro and in vivo, through gain- and loss-of-function studies. These studies have revealed physiological and pathophysiological influences on virtually every organ system and developmental stage of an organism. These include the nervous, cardiovascular, reproductive, and pulmonary systems. Disturbances in normal LPA signaling may contribute to a range of diseases, including neurodevelopmental and neuropsychiatric disorders, pain, cardiovascular disease, bone disorders, fibrosis, cancer, infertility, and obesity. These studies underscore the potential of LPA receptor subtypes and related signaling mechanisms to provide novel therapeutic targets.
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1 retracted
Lysophosphatidic Acid Stimulates the G-protein-coupled Receptor EDG-1 as a Low Affinity Agonist
Lee, M.-J., Thangada, S., Liu, C. H., Thompson, B. D., & Hla, T. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.34.22105 · Cited by 109
RetractedMembrane lipids: where they are and how they behave
van Meer, G., Voelker, D. R., & Feigenson, G. W. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2330 · Cited by 7,157
Isolation and Structure of a Brain Constituent That Binds to the Cannabinoid Receptor
Devane, W. A., Hanuš, L., Breuer, A., Pertwee, R. G., Stevenson, L. A., Griffin, G., Gibson, D., Mandelbaum, A., Etinger, A., & Mechoulam, R. (1992) · Science · doi:10.1126/science.1470919 · Cited by 5,633
Reilly, J. J., & Kelly, J. (2011) · International Journal of Obesity · doi:10.1038/ijo.2010.222 · Cited by 2,280
2-Arachidonoylgylcerol: A Possible Endogenous Cannabinoid Receptor Ligand in Brain
Sugiura, T., Kondo, S., Sukagawa, A., Nakane, S., Shinoda, A., Itoh, K., Yamashita, A., & Waku, K. (1995) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1995.2437 · Cited by 2,196
Regulation of the Hippo-YAP Pathway by G-Protein-Coupled Receptor Signaling
Yu, F.-X., Zhao, B., Panupinthu, N., Jewell, J. L., Lian, I., Wang, L. H., Zhao, J., Yuan, H., Tumaneng, K., Li, H., et al. (2012) · Cell · doi:10.1016/j.cell.2012.06.037 · Cited by 1,628
New roles for astrocytes: redefining the functional architecture of the brain.
Nedergaard, M., Ransom, B., & Goldman, S. A. (2003) · Trends in Neurosciences · doi:10.1016/j.tins.2003.08.008 · Cited by 1,334 · cited 1×
“Astrocytes are the most abundant type of glia and play a significant role in developmental, functional, and pathological processes (116).”
BackgroundUmezu-Goto, M., Kishi, Y., Taira, A., Hama, K., Dohmae, N., Takio, K., Yamori, T., Mills, G. B., Inoue, K., Aoki, J., et al. (2002) · The Journal of Cell Biology · doi:10.1083/jcb.200204026 · Cited by 929
LPA Receptors: Subtypes and Biological Actions
Choi, J. W., Herr, D. R., Noguchi, K., Yung, Y. C., Lee, C.-W., Mutoh, T., Lin, M.-E., Teo, S. T., Park, K. E., Mosley, A. N., et al. (2010) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.010909.105753 · Cited by 839
Self-citationvan Corven, E. J., Groenink, A., Jalink, K., Eichholtz, T., & Moolenaar, W. H. (1989) · Cell · doi:10.1016/0092-8674(89)90868-4 · Cited by 836
Cited by
Chun, J., Kihara, Y., Jonnalagadda, D., & Blaho, V. A. (2019) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-010818-021358 · Cited by 131
Self-citationPlastira, I., Bernhart, E., Goeritzer, M., Reicher, H., Kumble, V. B., Kogelnik, N., Wintersperger, A., Hammer, A., Schlager, S., Jandl, K., et al. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0701-9 · Cited by 112
Genome-wide CRISPR screening reveals genetic modifiers of mutant EGFR dependence in human NSCLC
Zeng, H., Castillo-Cabrera, J., Manser, M., Lu, B., Yang, Z., Strande, V., Begue, D., Zamponi, R., Qiu, S., Sigoillot, F., et al. (2019) · eLife · doi:10.7554/elife.50223 · Cited by 57
Autotaxin facilitates selective LPA receptor signaling
Salgado-Polo, F., Borza, R., Matsoukas, M.-T., Marsais, F., Jagerschmidt, C., Waeckel, L., Moolenaar, W. H., Ford, P., Heckmann, B., & Perrakis, A. (2023) · Cell Chemical Biology · doi:10.1016/j.chembiol.2022.12.006 · Cited by 45
Kanehira, M., Fujiwara, T., Nakajima, S., Okitsu, Y., Onishi, Y., Fukuhara, N., Ichinohasama, R., Okada, Y., & Harigae, H. (2017) · Stem Cells · doi:10.1002/stem.2499 · Cited by 42
Metadata
- Authors
- Yung, Y. C., Stoddard, N. C., & Chun, J.
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 55
- Issue
- 7
- Pages
- 1192-1214
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W2108812575
- Cited by
- 710
- References
- 263
- FWCI
- 16.18
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Yung, Y. C., Stoddard, N. C., & Chun, J. (2014). LPA receptor signaling: pharmacology, physiology, and pathophysiology. Journal of Lipid Research. https://doi.org/10.1194/jlr.r046458
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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.
