The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
Human Fibroblast Growth Factor-23 Mutants Suppress Na+-dependent Phosphate Co-transport Activity and 1α,25-Dihydroxyvitamin D3 Production
Open accessAbstract
The human fibroblast growth factor 23 (hFGF23) and its autosomal dominant hypophosphatemic rickets (ADHR) mutant genes were incorporated into animals by naked DNA injection to investigate the action on phosphate homeostasis in vivo. The hFGF23 mutants (R176Q, R179Q, and R179W) markedly reduced serum phosphorus (6.2-6.9 mg/dl) compared with the plasmid MOCK (8.5 mg/dl). However, native hFGF23 did not affect serum phosphorus (8.6 mg/dl). Both hFGF23 and hFGF23R179Q mRNAs were expressed more than 100-fold in the liver 4 days after injection, however, the C-terminal portion of hFGF23 was detected only in the serum from hFGF23R179Q-injected animals (1109 pg/ml). hFGF23R179Q mutant was secreted as a 32-kDa protein, whereas, native hFGF23 was detected as a 20-kDa protein in the cell-conditioned media. These results suggest the hFGF23R179Q protein is resistant to intracellular proteolytic processing. The hFGF23R179Q suppressed Na/P(i) co-transport activities both in kidney and in small intestine by 45 and 30%, respectively, as well as serum 1alpha,25-dihydroxyvitamin D(3) to less than 15 pg/ml. However, it had little effect on serum parathyroid hormone (PTH). Infusion of hFGF23R179Q protein normalized serum phosphorus in thyroparathyroidectomized rats without affecting serum calcium. Taken together, the FGF23 mutants reduce both phosphate uptake in intestine and phosphate reabsorption in kidney, independent of PTH action.
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Cites
Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23
White, K. E., Evans, W. E., O'Riordan, J. L. H., Speer, M. C., Econs, M. J., Lorenz-Depiereux, B., Grabowski, M., Meitinger, T., & Strom, T. M. (2000) · Nature Genetics · doi:10.1038/81664 · Cited by 1,528
Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia
Shimada, T., Mizutani, S., Muto, T., Yoneya, T., Hino, R., Takeda, S., Takeuchi, Y., Fujita, T., Fukumoto, S., & Yamashita, T. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.101545198 · Cited by 1,457
Yamashita, T., Yoshioka, M., & Itoh, N. (2000) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.2000.3696 · Cited by 554
Autosomal-dominant hypophosphatemic rickets (ADHR) mutations stabilize FGF-23
White, K. E., Carn, G., Lorenz-Depiereux, B., Benet-Pages, A., Strom, T. M., & Econs, M. J. (2001) · Kidney International · doi:10.1046/j.1523-1755.2001.00064.x · Cited by 493
Proximal Tubular Phosphate Reabsorption: Molecular Mechanisms
Murer, H., Hernando, N., Forster, I., & Biber, J. (2000) · Physiological Reviews · doi:10.1152/physrev.2000.80.4.1373 · Cited by 491
Jun-ichi, M., Satoshi, T., Kimi, A., Fumi, T., Akira, T., Kiyoshi, T., & Ken-ichi, Y. (1989) · Gene · doi:10.1016/0378-1119(89)90209-6 · Cited by 446
Shimada, T. (2002) · Endocrinology · doi:10.1210/en.143.8.3179 · Cited by 446
Animal Model of Adenine-Induced Chronic Renal Failure in Rats
Yokozawa, T., Zheng, P. D., Oura, H., & Koizumi, F. (1986) · Nephron · doi:10.1159/000183992 · Cited by 355
FGF-23 Inhibits Renal Tubular Phosphate Transport and Is a PHEX Substrate
Bowe, A. E., Finnegan, R., Jan de Beur, S. M., Cho, J., Levine, M. A., Kumar, R., & Schiavi, S. C. (2001) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.2001.5084 · Cited by 344
White, K. E. (2001) · Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.86.2.497 · Cited by 329
Cited by
The FGF family: biology, pathophysiology and therapy
Beenken, A., & Mohammadi, M. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2792 · Cited by 1,945
Regulation and Function of the FGF23/Klotho Endocrine Pathways
Martin, A., David, V., & Quarles, L. D. (2012) · Physiological Reviews · doi:10.1152/physrev.00002.2011 · Cited by 594
Ferrari, S. L., Bonjour, J.-P., & Rizzoli, R. (2005) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-1039 · Cited by 518
Endocrine functions of bone in mineral metabolism regulation
Quarles, L. D. (2008) · Journal of Clinical Investigation · doi:10.1172/jci36479 · Cited by 459
Regulation of C-Terminal and Intact FGF-23 by Dietary Phosphate in Men and Women
Burnett, S.-A. M., Gunawardene, S. C., Bringhurst, F. R., Jüppner, H., Lee, H., & Finkelstein, J. S. (2006) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.060507 · Cited by 455
Metadata
- Authors
- Saito, H., Kusano, K., Kinosaki, M., Ito, H., Hirata, M., Segawa, H., Miyamoto, K.-I., & Fukushima, N.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2003-01
- Volume
- 278
- Issue
- 4
- Pages
- 2206-2211
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1968779137
- Cited by
- 414
- References
- 21
- FWCI
- 14.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Saito, H., Kusano, K., Kinosaki, M., Ito, H., Hirata, M., Segawa, H., Miyamoto, K.-I., & Fukushima, N. (2003). Human Fibroblast Growth Factor-23 Mutants Suppress Na+-dependent Phosphate Co-transport Activity and 1α,25-Dihydroxyvitamin D3 Production. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m207872200
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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