Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo.
about
betaKlotho is required for fibroblast growth factor (FGF) 21 signaling through FGF receptor (FGFR) 1c and FGFR3cSecreted frizzled-related protein 4 is a potent tumor-derived phosphaturic agentHuman recombinant endopeptidase PHEX has a strict S1' specificity for acidic residues and cleaves peptides derived from fibroblast growth factor-23 and matrix extracellular phosphoglycoproteinFGF23-mediated regulation of systemic phosphate homeostasis: is Klotho an essential player?Molecular insights into the klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily membersMiscellaneous non-inflammatory musculoskeletal conditions. Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and αKlotho)Mucin-type O-glycosylation during developmentRegulation and function of the FGF23/klotho endocrine pathwaysExploring mechanisms of FGF signalling through the lens of structural biologyA potential link between phosphate and aging--lessons from Klotho-deficient miceThe autosomal dominant hypophosphatemic rickets R176Q mutation in fibroblast growth factor 23 resists proteolytic cleavage and enhances in vivo biological potencyHuman fibroblast growth factor-23 mutants suppress Na+-dependent phosphate co-transport activity and 1alpha,25-dihydroxyvitamin D3 productionMolecular mechanisms of fibroblast growth factor signaling in physiology and pathologyRationale-Based Engineering of a Potent Long-Acting FGF21 Analog for the Treatment of Type 2 DiabetesHomozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient miceRegulation of fibroblast growth factor-23 signaling by klothoTargeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolismIsolated C-terminal tail of FGF23 alleviates hypophosphatemia by inhibiting FGF23-FGFR-Klotho complex formation.Circulating fibroblast growth factor 23 in patients with end-stage renal disease treated by peritoneal dialysis is intact and biologically activeFGF23 is synthesised locally by renal tubules and activates injury-primed fibroblasts.The use of fibroblast growth factor 23 testing in patients with kidney disease.Urinary prostaglandins and the effect of indomethacin on phosphate excretion in children with hypophosphatemic rickets.Phosphate-induced apoptosis of hypertrophic chondrocytes is associated with a decrease in mitochondrial membrane potential and is dependent upon Erk1/2 phosphorylation.Fibroblast growth factor-23 increases mouse PGE2 production in vivo and in vitro.Mineral metabolism and aging: the fibroblast growth factor 23 enigma.FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1.Phosphatonin washout in Hyp mice proximal tubules: evidence for posttranscriptional regulation.Hypophosphatemic rickets: revealing novel control points for phosphate homeostasis.Genetic rescue of glycosylation-deficient Fgf23 in the Galnt3 knockout mouse.The changing face of hypophosphatemic disorders in the FGF-23 eraFGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wastingFibroblast growth factor 23 contributes to diminished bone mineral density in childhood inflammatory bowel disease.Recent advances in renal phosphate handling.Plasma fibroblast growth factor 23 concentration is increased and predicts mortality in patients on the liver-transplant waiting list.FGF-23 regulates CYP27B1 transcription in the kidney and in extra-renal tissues.The roles of the skeleton and phosphorus in the CKD mineral bone disorderCoupling fibroblast growth factor 23 production and cleavage: iron deficiency, rickets, and kidney disease.Evaluation of a method for fibroblast growth factor-23: a novel biomarker of adverse outcomes in patients with renal disease.Regulation of phosphate transport by fibroblast growth factor 23 (FGF23): implications for disorders of phosphate metabolism.FGF-23: More than a regulator of renal phosphate handling?
P2860
Q24306279-FAE044AD-7E3F-4DCC-9539-519CACBD8116Q24319643-AC62B15F-CEE8-4C7E-A8BF-8D749422ADBCQ24530025-08DF6A34-6394-4DFB-B497-1DDF2D8B41EDQ24653541-900ED696-FEB5-4E29-8D3B-35861ADBD06AQ24683254-4ABADF0E-80D6-4641-BC55-CEE9F2FE5453Q26827280-15CAFA33-E857-40AF-8DEB-E8F24A77A2F7Q26849608-9CDD14BB-B623-4C03-A690-9547B15CDEE2Q26860470-B4BDE236-195F-4B01-B843-F25E230E4F50Q27015054-F20F7763-31D0-495E-AC35-372F969E2D23Q27687316-2563BA10-29E1-405B-AEC9-EF798C2E37CBQ28202356-1C4E6485-B57A-4549-99E4-71BBA340FDE8Q28213962-429F6F85-A9BE-4D18-82D6-1BEC7E97FB83Q28291993-8748A759-A08F-4C54-AB72-CA9FCE236B76Q28485340-4CA89548-6769-426B-8C87-57C2B50E94CDQ28507303-238BB693-BFD3-48B8-8473-198814C3D3D2Q28587100-A10E4166-AD74-4558-AD12-532DB792EEE3Q29620323-B0821E78-5D5B-43F6-87AE-A442BC7FEB82Q33591785-062F270C-D2C9-4B8E-A973-6FFB7467450CQ33736093-980E1E1E-EBD4-4BED-AD56-E8244927BDCBQ33793927-B1BE926E-D360-4B06-93A2-528F1113AD0AQ33835743-51733F36-2888-4DB3-AD98-46DBD9566738Q33897553-AEF64FCD-AC37-4224-A2F4-8D79D0029919Q33897727-421AD403-AE37-45BE-9856-445020693017Q33897866-60CCDD36-1B4B-42C0-BAF8-3CD411573F86Q33982618-50A20D6F-7CEE-46BA-9372-DABD3AF9E4E2Q34017992-DF3242F9-EA2C-420D-BBA2-F475E9CC653DQ34030128-5D0E79D7-58B9-4761-A351-9DD7BD2D7D89Q34069793-0EF75396-E2BF-4F2D-8043-B83EF4EC2D13Q34185739-3DA2C1F6-52F9-4461-A992-9678686D5F5BQ34221238-7FCD0713-E180-4D5F-8811-63A46250C30AQ34227442-10252B6F-17C2-4AF1-AE51-F42674B9DDE4Q34253710-A60B90C6-A535-4CD7-AFFF-AE0A51764152Q34631794-F130D30A-3D61-4DD9-BADB-9EE04E726190Q34794004-93AC7E6E-E67E-4439-B318-7706B6BCCA11Q34982729-04D1E736-52AD-4231-A05D-30569C335124Q35013304-7277C72F-A89C-4F78-AF93-B02F260867CBQ35067500-F60DF1B6-1C10-482D-BF4F-0191C272A2EDQ35075064-1DA8BB4A-B706-48CF-82B5-4C495E55639CQ35151453-CEAB4535-735D-4685-9427-2D62C12AF25DQ35156017-42E8E00F-C770-4A7E-ADED-40173A9AF681
P2860
Mutant FGF-23 responsible for autosomal dominant hypophosphatemic rickets is resistant to proteolytic cleavage and causes hypophosphatemia in vivo.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
@wuu
2002年学术文章
@zh-cn
2002年学术文章
@zh-hans
2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
@yue
2002年學術文章
@zh
2002年學術文章
@zh-hant
name
Mutant FGF-23 responsible for ...... uses hypophosphatemia in vivo.
@en
Mutant FGF-23 responsible for ...... uses hypophosphatemia in vivo.
@nl
type
label
Mutant FGF-23 responsible for ...... uses hypophosphatemia in vivo.
@en
Mutant FGF-23 responsible for ...... uses hypophosphatemia in vivo.
@nl
prefLabel
Mutant FGF-23 responsible for ...... uses hypophosphatemia in vivo.
@en
Mutant FGF-23 responsible for ...... uses hypophosphatemia in vivo.
@nl
P2093
P356
P1433
P1476
Mutant FGF-23 responsible for ...... uses hypophosphatemia in vivo.
@en
P2093
Itaru Urakawa
Katsuya Okawa
Seiji Fukumoto
Takanori Muto
Takashi Shimada
Takashi Yoneya
Takeyoshi Yamashita
Toshiro Fujita
Yasuhiro Takeuchi
Yuji Yamazaki
P304
P356
10.1210/EN.143.8.3179
P407
P577
2002-08-01T00:00:00Z