The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Characterization of lpa2 (Edg4) and lpa1/lpa2 (Edg2/Edg4) Lysophosphatidic Acid Receptor Knockout Mice: Signaling Deficits without Obvious Phenotypic Abnormality Attributable to lpa2
Open accessAbstract
Lysophosphatidic acid (LPA), a bioactive lipid produced by several cell types including postmitotic neurons and activated platelets, is thought to be involved in various biological processes, including brain development. Three cognate G protein-coupled receptors encoded by lpa(1)/lp(A1)/Edg-2/Gpcr26, lpa(2)/lp(A2)/Edg-4, and lpa(3)/lp(A3)/Edg-7 mediate the cellular effects of LPA. We have previously shown that deletion of lpa(1) in mice results in craniofacial dysmorphism, semilethality due to defective suckling behavior, and generation of a small fraction of pups with frontal hematoma. To further investigate the role of these receptors and LPA signaling in the organism, we deleted lpa(2) in mice. Homozygous knockout (lpa(2)((-/-))) mice were born at the expected frequency and displayed no obvious phenotypic abnormalities. Intercrosses allowed generation of lpa(1)((-/-)) lpa(2)((-/-)) double knockout mice, which displayed no additional phenotypic abnormalities relative to lpa(1)((-/-)) mice except for an increased incidence of perinatal frontal hematoma. Histological analyses of lpa(1)((-/-)) lpa(2)((-/-)) embryonic cerebral cortices did not reveal obvious differences in the proliferating cell population. However, many LPA-induced responses, including phospholipase C activation, Ca(2+) mobilization, adenylyl cyclase activation, proliferation, JNK activation, Akt activation, and stress fiber formation, were absent or severely reduced in embryonic fibroblasts derived from lpa(1)((-/-)) lpa(2)((-/-)) mice. Except for adenylyl cyclase activation [which was nearly abolished in lpa(1)((-/-)) fibroblasts], these responses were only partially affected in lpa(1)((-/-)) and lpa(2)((-/-)) fibroblasts. Thus, although LPA(2) is not essential for normal mouse development, it does act redundantly with LPA(1) to mediate most LPA responses in fibroblasts.
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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
RetractedRidley, A. J., & Hall, A. (1992) · Cell · doi:10.1016/0092-8674(92)90163-7 · Cited by 4,468
van 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
Hecht, J. H., Weiner, J. A., Post, S. R., & Chun, J. (1996) · The Journal of cell biology · doi:10.1083/jcb.135.4.1071 · Cited by 720
Self-citationThe bioactive phospholipid lysophosphatidic acid is released from activated platelets
Eichholtz, T., Jalink, K., Fahrenfort, I., & Moolenaar, W. H. (1993) · Biochemical Journal · doi:10.1042/bj2910677 · Cited by 645
Blaschke, A. J., Staley, K., & Chun, J. (1996) · Development · doi:10.1242/dev.122.4.1165 · Cited by 531
Self-citationCharacterization of a Novel Subtype of Human G Protein-coupled Receptor for Lysophosphatidic Acid
An, S., Bleu, T., Hallmark, O. G., & Goetzl, E. J. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.14.7906 · Cited by 528
Bandoh, K., Aoki, J., Hosono, H., Kobayashi, S., Kobayashi, T., Murakami-Murofushi, K., Tsujimoto, M., Arai, H., & Inoue, K. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.39.27776 · Cited by 511
Lysophosphatidic acid: G-protein signalling and cellular responses
Moolenaar, W. H., Kranenburg, O., Postma, F. R., & Zondag, G. C. (1997) · Current Opinion in Cell Biology · doi:10.1016/s0955-0674(97)80059-2 · Cited by 486
Requirement for the lp A1 lysophosphatidic acid receptor gene in normal suckling behavior
Contos, J. J. A., Fukushima, N., Weiner, J. A., Kaushal, D., & Chun, J. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.97.24.13384 · Cited by 479
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Cited by
Lysophospholipid Receptors: Signaling and Biology
Ishii, I., Fukushima, N., Ye, X., & Chun, J. (2004) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.73.011303.073731 · Cited by 771
Self-citationLysophospholipid receptors: Signalling, pharmacology and regulation by lysophospholipid metabolism
Meyer zu Heringdorf, D., & Jakobs, K. H. (2007) · Biochimica et Biophysica Acta (BBA) - Biomembranes · doi:10.1016/j.bbamem.2006.09.026 · Cited by 388
Regulation and biological activities of the autotaxin–LPA axis
van Meeteren, L. A., & Moolenaar, W. H. (2007) · Progress in Lipid Research · doi:10.1016/j.plipres.2007.02.001 · Cited by 353
Mutant G-protein-coupled receptors as a cause of human diseases
Schöneberg, T., Schulz, A., Biebermann, H., Hermsdorf, T., Römpler, H., & Sangkuhl, K. (2004) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2004.08.008 · Cited by 337
Lysophospholipids and their receptors in the central nervous system
Choi, J. W., & Chun, J. (2013) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2012.07.015 · Cited by 255
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Metadata
- Authors
- Contos, J. J. A., Ishii, I., Fukushima, N., Kingsbury, M. A., Ye, X., Kawamura, S., Brown, J. H., & Chun, J.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2002-10-01
- Volume
- 22
- Issue
- 19
- Pages
- 6921-6929
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2156303710
- Cited by
- 316
- References
- 35
- FWCI
- 5.29
- Type
- journal article
- Language
- en
- Open access
- green
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