Peter S N Rowe's Laboratory Page

1. Rowe, P.S.N., et al., Surface Plasmon Resonance (SPR) confirms MEPE binds to PHEX via the MEPE-ASARM-motif: A model for impaired mineralization in X-linked rickets (Hyp). 2004. Submitted.

2. Rowe, P.S.N., et al., MEPE has the properties of an osteoblastic Phosphatonin and Minhibin. Bone, 2004. 34(2): p. 303-319.

3. Rowe, P.S.N., The wrickkened-pathways of FGF23, MEPE and PHEX. Critical Reviews in Oral Biology & Medicine, 2004.
15: p.264-81.

4. Guo, R., et al., Inhibition of MEPE cleavage by Phex. Biochem Biophys Res Commun, 2002. 297(1): p. 38-45.

5. Rowe, P.S., The molecular background to hypophosphataemic rickets. Arch.Dis.Child 2000.Sep.;83.(3.):192.-4., 2000. 83: p. 192-194.

6. Rowe, P.S.N., Finding Mutations in Disease Genes, in Genetics of Osteoporosis and Metabolic Bone Disease, M.J. Econs, Editor. 2000, Humana Press Inc: Totowa New Jersey. p. 431-446.

7. Rowe, P.S.N., et al., MEPE, a new gene expressed in bone-marrow and tumours causing osteomalacia. Genomics., 2000. 67 (1): p. 54-68.

8. Rowe, P.S.N., X-linked rickets and tumour osteomalacia: PHEX and the missing link. Clinical and Experimental Nephrology, 1998. 2(3): p. 183-193.

9. Rowe, P.S.N., The role of the PHEX gene (PEX), in families with X-linked hypophosphataemic rickets. Current Opinion in Nephrology & Hypertension, 1998. 7(4): p. 367-376.

10. Rowe, P.S., The PEX gene: its role in X-linked rickets, osteomalacia, and bone mineral metabolism. Exp Nephrol., 1997. 5: p. 355-363.

11. HYP-consortium, et al., A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. The HYP Consortium. Nat.Genet., 1995. 11: p. 130-136.

12. Rowe, P.S.N., et al., Distribution of mutations in the PEX gene in families with X-linked hypophosphataemic rickets (HYP). Hum.Mol.Genet., 1997. 6: p. 539-549.

13. Rowe, P.S.N., et al., Candidate 56 and 58 kDa protein(s) responsible for mediating the renal defects in oncogenic hypophosphataemic osteomalacia. Bone., 1996. 18(2): p. 159-169.


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Peter S N Rowe's Laboratory Page

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Selected References: 1. Rowe, P.S.N., et al., Surface Plasmon Resonance (SPR) confirms MEPE binds to PHEX via the MEPE-ASARM-motif: A model for impaired mineralization in X-linked rickets (Hyp). 2004. Submitted. 2. Rowe, P.S.N., et al., MEPE has the properties of an osteoblastic Phosphatonin and Minhibin. Bone, 2004. 34(2): p. 303-319. 3. Rowe, P.S.N., The wrickkened-pathways of FGF23, MEPE and PHEX. Critical Reviews in Oral Biology & Medicine, 2004. 15: p.264-81. 4. Guo, R., et al., Inhibition of MEPE cleavage by Phex. Biochem Biophys Res Commun, 2002. 297(1): p. 38-45. 5. Rowe, P.S., The molecular background to hypophosphataemic rickets. Arch.Dis.Child 2000.Sep.;83.(3.):192.-4., 2000. 83: p. 192-194. 6. Rowe, P.S.N., Finding Mutations in Disease Genes, in Genetics of Osteoporosis and Metabolic Bone Disease, M.J. Econs, Editor. 2000, Humana Press Inc: Totowa New Jersey. p. 431-446. 7. Rowe, P.S.N., et al., MEPE, a new gene expressed in bone-marrow and tumours causing osteomalacia. Genomics., 2000. 67 (1): p. 54-68. 8. Rowe, P.S.N., X-linked rickets and tumour osteomalacia: PHEX and the missing link. Clinical and Experimental Nephrology, 1998. 2(3): p. 183-193. 9. Rowe, P.S.N., The role of the PHEX gene (PEX), in families with X-linked hypophosphataemic rickets. Current Opinion in Nephrology & Hypertension, 1998. 7(4): p. 367-376. 10. Rowe, P.S., The PEX gene: its role in X-linked rickets, osteomalacia, and bone mineral metabolism. Exp Nephrol., 1997. 5: p. 355-363. 11. HYP-consortium, et al., A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets. The HYP Consortium. Nat.Genet., 1995. 11: p. 130-136. 12. Rowe, P.S.N., et al., Distribution of mutations in the PEX gene in families with X-linked hypophosphataemic rickets (HYP). Hum.Mol.Genet., 1997. 6: p. 539-549. 13. Rowe, P.S.N., et al., Candidate 56 and 58 kDa protein(s) responsible for mediating the renal defects in oncogenic hypophosphataemic osteomalacia. Bone., 1996. 18(2): p. 159-169.