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Florence W L Tsui - One of the best experts on this subject based on the ideXlab platform.

  • the cppdd associated ankh m48t mutation interrupts the interaction of ankh with the sodium Phosphate cotransporter pit 1
    The Journal of Rheumatology, 2009
    Co-Authors: John L Wang, Frank Beier, Hing Wo Tsui, Florence W L Tsui
    Abstract:

    Objective. Numerous dominant human homolog of progressive ankylosis ( ANKH ) mutations have been identified in familial calcium pyroPhosphate dihydrate crystal deposition disease (CPPDD). Due to the dominant nature of these mutations, we investigated whether ANKH interacts with other proteins; and if so, whether any CPPDD-associated ANKH mutation might disrupt such protein interactions. Methods. Stable ATDC5 ANKH wt- and ANKH M48T- transfectants were generated. Lysates from these transfectants were used to identify candidate protein interaction with ANKH by coimmunoprecipitation followed by Western blot analysis. The effect of high Phosphate on the expression of genes involved in modulating Pi (inorganic Phosphate)/PPi (inorganic pyroPhosphate) homeostasis in these transfectants was assessed. Results. We showed that ANKH protein associates with the sodium/Phosphate cotransporter PiT-1, and that ANKH M48T mutant protein failed to interact with PiT-1. We also showed that upon high Phosphate Treatment, the normally coordinated upregulation of endogenous Ank and PiT1 transcript expression was disrupted in ANKH M48T transfectants. Conclusion Our results suggested that there is a coordinated interrelationship between 2 key participants of Pi and PPi metabolism, ANKH and PiT-1.

  • The CPPDD-Associated ANKH M48T Mutation Interrupts the Interaction of ANKH with the Sodium/Phosphate Cotransporter PiT-1
    The Journal of Rheumatology, 2009
    Co-Authors: John L Wang, Frank Beier, Hing Wo Tsui, Florence W L Tsui
    Abstract:

    Objective. Numerous dominant human homolog of progressive ankylosis ( ANKH ) mutations have been identified in familial calcium pyroPhosphate dihydrate crystal deposition disease (CPPDD). Due to the dominant nature of these mutations, we investigated whether ANKH interacts with other proteins; and if so, whether any CPPDD-associated ANKH mutation might disrupt such protein interactions. Methods. Stable ATDC5 ANKH wt- and ANKH M48T- transfectants were generated. Lysates from these transfectants were used to identify candidate protein interaction with ANKH by coimmunoprecipitation followed by Western blot analysis. The effect of high Phosphate on the expression of genes involved in modulating Pi (inorganic Phosphate)/PPi (inorganic pyroPhosphate) homeostasis in these transfectants was assessed. Results. We showed that ANKH protein associates with the sodium/Phosphate cotransporter PiT-1, and that ANKH M48T mutant protein failed to interact with PiT-1. We also showed that upon high Phosphate Treatment, the normally coordinated upregulation of endogenous Ank and PiT1 transcript expression was disrupted in ANKH M48T transfectants. Conclusion Our results suggested that there is a coordinated interrelationship between 2 key participants of Pi and PPi metabolism, ANKH and PiT-1.

John L Wang - One of the best experts on this subject based on the ideXlab platform.

  • the cppdd associated ankh m48t mutation interrupts the interaction of ankh with the sodium Phosphate cotransporter pit 1
    The Journal of Rheumatology, 2009
    Co-Authors: John L Wang, Frank Beier, Hing Wo Tsui, Florence W L Tsui
    Abstract:

    Objective. Numerous dominant human homolog of progressive ankylosis ( ANKH ) mutations have been identified in familial calcium pyroPhosphate dihydrate crystal deposition disease (CPPDD). Due to the dominant nature of these mutations, we investigated whether ANKH interacts with other proteins; and if so, whether any CPPDD-associated ANKH mutation might disrupt such protein interactions. Methods. Stable ATDC5 ANKH wt- and ANKH M48T- transfectants were generated. Lysates from these transfectants were used to identify candidate protein interaction with ANKH by coimmunoprecipitation followed by Western blot analysis. The effect of high Phosphate on the expression of genes involved in modulating Pi (inorganic Phosphate)/PPi (inorganic pyroPhosphate) homeostasis in these transfectants was assessed. Results. We showed that ANKH protein associates with the sodium/Phosphate cotransporter PiT-1, and that ANKH M48T mutant protein failed to interact with PiT-1. We also showed that upon high Phosphate Treatment, the normally coordinated upregulation of endogenous Ank and PiT1 transcript expression was disrupted in ANKH M48T transfectants. Conclusion Our results suggested that there is a coordinated interrelationship between 2 key participants of Pi and PPi metabolism, ANKH and PiT-1.

  • The CPPDD-Associated ANKH M48T Mutation Interrupts the Interaction of ANKH with the Sodium/Phosphate Cotransporter PiT-1
    The Journal of Rheumatology, 2009
    Co-Authors: John L Wang, Frank Beier, Hing Wo Tsui, Florence W L Tsui
    Abstract:

    Objective. Numerous dominant human homolog of progressive ankylosis ( ANKH ) mutations have been identified in familial calcium pyroPhosphate dihydrate crystal deposition disease (CPPDD). Due to the dominant nature of these mutations, we investigated whether ANKH interacts with other proteins; and if so, whether any CPPDD-associated ANKH mutation might disrupt such protein interactions. Methods. Stable ATDC5 ANKH wt- and ANKH M48T- transfectants were generated. Lysates from these transfectants were used to identify candidate protein interaction with ANKH by coimmunoprecipitation followed by Western blot analysis. The effect of high Phosphate on the expression of genes involved in modulating Pi (inorganic Phosphate)/PPi (inorganic pyroPhosphate) homeostasis in these transfectants was assessed. Results. We showed that ANKH protein associates with the sodium/Phosphate cotransporter PiT-1, and that ANKH M48T mutant protein failed to interact with PiT-1. We also showed that upon high Phosphate Treatment, the normally coordinated upregulation of endogenous Ank and PiT1 transcript expression was disrupted in ANKH M48T transfectants. Conclusion Our results suggested that there is a coordinated interrelationship between 2 key participants of Pi and PPi metabolism, ANKH and PiT-1.

Hing Wo Tsui - One of the best experts on this subject based on the ideXlab platform.

  • the cppdd associated ankh m48t mutation interrupts the interaction of ankh with the sodium Phosphate cotransporter pit 1
    The Journal of Rheumatology, 2009
    Co-Authors: John L Wang, Frank Beier, Hing Wo Tsui, Florence W L Tsui
    Abstract:

    Objective. Numerous dominant human homolog of progressive ankylosis ( ANKH ) mutations have been identified in familial calcium pyroPhosphate dihydrate crystal deposition disease (CPPDD). Due to the dominant nature of these mutations, we investigated whether ANKH interacts with other proteins; and if so, whether any CPPDD-associated ANKH mutation might disrupt such protein interactions. Methods. Stable ATDC5 ANKH wt- and ANKH M48T- transfectants were generated. Lysates from these transfectants were used to identify candidate protein interaction with ANKH by coimmunoprecipitation followed by Western blot analysis. The effect of high Phosphate on the expression of genes involved in modulating Pi (inorganic Phosphate)/PPi (inorganic pyroPhosphate) homeostasis in these transfectants was assessed. Results. We showed that ANKH protein associates with the sodium/Phosphate cotransporter PiT-1, and that ANKH M48T mutant protein failed to interact with PiT-1. We also showed that upon high Phosphate Treatment, the normally coordinated upregulation of endogenous Ank and PiT1 transcript expression was disrupted in ANKH M48T transfectants. Conclusion Our results suggested that there is a coordinated interrelationship between 2 key participants of Pi and PPi metabolism, ANKH and PiT-1.

  • The CPPDD-Associated ANKH M48T Mutation Interrupts the Interaction of ANKH with the Sodium/Phosphate Cotransporter PiT-1
    The Journal of Rheumatology, 2009
    Co-Authors: John L Wang, Frank Beier, Hing Wo Tsui, Florence W L Tsui
    Abstract:

    Objective. Numerous dominant human homolog of progressive ankylosis ( ANKH ) mutations have been identified in familial calcium pyroPhosphate dihydrate crystal deposition disease (CPPDD). Due to the dominant nature of these mutations, we investigated whether ANKH interacts with other proteins; and if so, whether any CPPDD-associated ANKH mutation might disrupt such protein interactions. Methods. Stable ATDC5 ANKH wt- and ANKH M48T- transfectants were generated. Lysates from these transfectants were used to identify candidate protein interaction with ANKH by coimmunoprecipitation followed by Western blot analysis. The effect of high Phosphate on the expression of genes involved in modulating Pi (inorganic Phosphate)/PPi (inorganic pyroPhosphate) homeostasis in these transfectants was assessed. Results. We showed that ANKH protein associates with the sodium/Phosphate cotransporter PiT-1, and that ANKH M48T mutant protein failed to interact with PiT-1. We also showed that upon high Phosphate Treatment, the normally coordinated upregulation of endogenous Ank and PiT1 transcript expression was disrupted in ANKH M48T transfectants. Conclusion Our results suggested that there is a coordinated interrelationship between 2 key participants of Pi and PPi metabolism, ANKH and PiT-1.

Frank Beier - One of the best experts on this subject based on the ideXlab platform.

  • the cppdd associated ankh m48t mutation interrupts the interaction of ankh with the sodium Phosphate cotransporter pit 1
    The Journal of Rheumatology, 2009
    Co-Authors: John L Wang, Frank Beier, Hing Wo Tsui, Florence W L Tsui
    Abstract:

    Objective. Numerous dominant human homolog of progressive ankylosis ( ANKH ) mutations have been identified in familial calcium pyroPhosphate dihydrate crystal deposition disease (CPPDD). Due to the dominant nature of these mutations, we investigated whether ANKH interacts with other proteins; and if so, whether any CPPDD-associated ANKH mutation might disrupt such protein interactions. Methods. Stable ATDC5 ANKH wt- and ANKH M48T- transfectants were generated. Lysates from these transfectants were used to identify candidate protein interaction with ANKH by coimmunoprecipitation followed by Western blot analysis. The effect of high Phosphate on the expression of genes involved in modulating Pi (inorganic Phosphate)/PPi (inorganic pyroPhosphate) homeostasis in these transfectants was assessed. Results. We showed that ANKH protein associates with the sodium/Phosphate cotransporter PiT-1, and that ANKH M48T mutant protein failed to interact with PiT-1. We also showed that upon high Phosphate Treatment, the normally coordinated upregulation of endogenous Ank and PiT1 transcript expression was disrupted in ANKH M48T transfectants. Conclusion Our results suggested that there is a coordinated interrelationship between 2 key participants of Pi and PPi metabolism, ANKH and PiT-1.

  • The CPPDD-Associated ANKH M48T Mutation Interrupts the Interaction of ANKH with the Sodium/Phosphate Cotransporter PiT-1
    The Journal of Rheumatology, 2009
    Co-Authors: John L Wang, Frank Beier, Hing Wo Tsui, Florence W L Tsui
    Abstract:

    Objective. Numerous dominant human homolog of progressive ankylosis ( ANKH ) mutations have been identified in familial calcium pyroPhosphate dihydrate crystal deposition disease (CPPDD). Due to the dominant nature of these mutations, we investigated whether ANKH interacts with other proteins; and if so, whether any CPPDD-associated ANKH mutation might disrupt such protein interactions. Methods. Stable ATDC5 ANKH wt- and ANKH M48T- transfectants were generated. Lysates from these transfectants were used to identify candidate protein interaction with ANKH by coimmunoprecipitation followed by Western blot analysis. The effect of high Phosphate on the expression of genes involved in modulating Pi (inorganic Phosphate)/PPi (inorganic pyroPhosphate) homeostasis in these transfectants was assessed. Results. We showed that ANKH protein associates with the sodium/Phosphate cotransporter PiT-1, and that ANKH M48T mutant protein failed to interact with PiT-1. We also showed that upon high Phosphate Treatment, the normally coordinated upregulation of endogenous Ank and PiT1 transcript expression was disrupted in ANKH M48T transfectants. Conclusion Our results suggested that there is a coordinated interrelationship between 2 key participants of Pi and PPi metabolism, ANKH and PiT-1.

Etienne Sochett - One of the best experts on this subject based on the ideXlab platform.

  • prolonged high dose Phosphate Treatment a risk factor for tertiary hyperparathyroidism in x linked hypoPhosphatemic rickets
    Clinical Endocrinology, 2003
    Co-Authors: Outi Makitie, Sang Whay Kooh, Etienne Sochett
    Abstract:

    Summary objective X-linked hypoPhosphatemic rickets is characterized by renal Phosphate wasting, hypoPhosphatemia and defective bone mineralization. Treatment with oral Phosphate (Pi) and calcitriol improves skeletal changes but associates with secondary hyperparathyroidism and nephrocalcinosis. Tertiary hyperparathyroidism is a rare complication of the Treatment. The aim of the present study was to identify Treatment-related factors that might be associated with the transition of secondary hyperparathyroidism to tertiary hyperparathyroidism in patients with X-linked hypoPhosphatemic rickets. design Thirteen patients with X-linked hypoPhosphatemic rickets and secondary or tertiary hyperparathyroidism were included in the study. Their hospital records were reviewed and compared for onset, duration and dosage of Treatment, and for age of diagnosis and degree of secondary hyperparathyroidism. results Two patients developed tertiary hyperparathyroidism and 11 patients secondary hyperparathyroidism during the Treatment. Patients with tertiary hyperparathyroidism had, on average, earlier onset and longer duration of Treatment, higher dose of Pi and longer duration of Treatment with very high Pi doses (> 100 mg/kg/day) compared to the 11 patients with secondary hyperparathyroidism. However, variation of all parameters was great with considerable overlap. Very high S-PTH levels ≥ 42 pmol/l were observed in those who later developed tertiary hyperparathyroidism. conclusions Prolonged very high dose oral Pi Treatment is a major risk factor for the development of tertiary hyperparathyroidism in X-linked hypoPhosphatemic rickets.