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Parathyroid cell resistance to fibroblast growth factor 23 in secondary hyperparathyroidism of chronic kidney disease
by
Ben-Dov, I.Z.
, Galitzer, H.
, Silver, Justin
, Naveh-Many, Tally
in
Adenine - toxicity
/ Animals
/ Biological and medical sciences
/ Chronic Disease
/ chronic renal failure
/ Down-Regulation - genetics
/ Endocrinopathies
/ Fibroblast Growth Factors - analysis
/ Fibroblast Growth Factors - physiology
/ gene expression
/ Glucuronidase - analysis
/ hyperparathyroidism
/ Hyperparathyroidism, Secondary - genetics
/ Kidney Diseases - chemically induced
/ Kidney Diseases - complications
/ Kidneys
/ Medical sciences
/ Nephrology. Urinary tract diseases
/ Non tumoral diseases. Target tissue resistance. Benign neoplasms
/ Parathyroid Glands - chemistry
/ parathyroid hormone
/ Parathyroid Hormone - analysis
/ Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases)
/ Rats
/ Receptor, Fibroblast Growth Factor, Type 1 - analysis
/ RNA, Messenger - analysis
/ Urinary system involvement in other diseases. Miscellaneous
2010
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Parathyroid cell resistance to fibroblast growth factor 23 in secondary hyperparathyroidism of chronic kidney disease
by
Ben-Dov, I.Z.
, Galitzer, H.
, Silver, Justin
, Naveh-Many, Tally
in
Adenine - toxicity
/ Animals
/ Biological and medical sciences
/ Chronic Disease
/ chronic renal failure
/ Down-Regulation - genetics
/ Endocrinopathies
/ Fibroblast Growth Factors - analysis
/ Fibroblast Growth Factors - physiology
/ gene expression
/ Glucuronidase - analysis
/ hyperparathyroidism
/ Hyperparathyroidism, Secondary - genetics
/ Kidney Diseases - chemically induced
/ Kidney Diseases - complications
/ Kidneys
/ Medical sciences
/ Nephrology. Urinary tract diseases
/ Non tumoral diseases. Target tissue resistance. Benign neoplasms
/ Parathyroid Glands - chemistry
/ parathyroid hormone
/ Parathyroid Hormone - analysis
/ Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases)
/ Rats
/ Receptor, Fibroblast Growth Factor, Type 1 - analysis
/ RNA, Messenger - analysis
/ Urinary system involvement in other diseases. Miscellaneous
2010
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Parathyroid cell resistance to fibroblast growth factor 23 in secondary hyperparathyroidism of chronic kidney disease
by
Ben-Dov, I.Z.
, Galitzer, H.
, Silver, Justin
, Naveh-Many, Tally
in
Adenine - toxicity
/ Animals
/ Biological and medical sciences
/ Chronic Disease
/ chronic renal failure
/ Down-Regulation - genetics
/ Endocrinopathies
/ Fibroblast Growth Factors - analysis
/ Fibroblast Growth Factors - physiology
/ gene expression
/ Glucuronidase - analysis
/ hyperparathyroidism
/ Hyperparathyroidism, Secondary - genetics
/ Kidney Diseases - chemically induced
/ Kidney Diseases - complications
/ Kidneys
/ Medical sciences
/ Nephrology. Urinary tract diseases
/ Non tumoral diseases. Target tissue resistance. Benign neoplasms
/ Parathyroid Glands - chemistry
/ parathyroid hormone
/ Parathyroid Hormone - analysis
/ Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases)
/ Rats
/ Receptor, Fibroblast Growth Factor, Type 1 - analysis
/ RNA, Messenger - analysis
/ Urinary system involvement in other diseases. Miscellaneous
2010
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Parathyroid cell resistance to fibroblast growth factor 23 in secondary hyperparathyroidism of chronic kidney disease
Journal Article
Parathyroid cell resistance to fibroblast growth factor 23 in secondary hyperparathyroidism of chronic kidney disease
2010
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Overview
Although fibroblast growth factor 23 (FGF23) acting through its receptor Klotho-FGFR1c decreases parathyroid hormone expression, this hormone is increased in chronic kidney disease despite an elevated serum FGF23. We measured possible factors that might contribute to the resistance of parathyroid glands to FGF23 in rats with the dietary adenine-induced model of chronic kidney disease. Quantitative immunohistochemical and reverse transcription–PCR analysis using laser capture microscopy showed that both Klotho and FGFR1 protein and mRNA levels were decreased in histological sections of the parathyroid glands. Recombinant FGF23 failed to decrease serum parathyroid hormone levels or activate the mitogen-activated protein kinase signaling pathway in the glands of rats with advanced experimental chronic kidney disease. In parathyroid gland organ culture, the addition of FGF23 decreased parathyroid hormone secretion and mRNA levels in control animals or rats with early but not advanced chronic kidney disease. Our results show that because of a downregulation of the Klotho–FGFR1c receptor complex, an increase of circulating FGF23 does not decrease parathyroid hormone levels in established chronic kidney disease. This in vivo resistance is sustained in parathyroid organ culture in vitro.
Publisher
Elsevier Inc,Nature Publishing Group,Elsevier Limited
Subject
/ Animals
/ Biological and medical sciences
/ Fibroblast Growth Factors - analysis
/ Fibroblast Growth Factors - physiology
/ Hyperparathyroidism, Secondary - genetics
/ Kidney Diseases - chemically induced
/ Kidney Diseases - complications
/ Kidneys
/ Nephrology. Urinary tract diseases
/ Non tumoral diseases. Target tissue resistance. Benign neoplasms
/ Parathyroid Glands - chemistry
/ Parathyroid Hormone - analysis
/ Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases)
/ Rats
/ Receptor, Fibroblast Growth Factor, Type 1 - analysis
/ Urinary system involvement in other diseases. Miscellaneous
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