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Titlebook: G Proteins, Receptors, and Disease; Allen M. Spiegel (Chief, Metabolic Diseases Branch Book 1998 Springer Science+Business Media New York

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發(fā)表于 2025-3-25 06:19:01 | 只看該作者
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發(fā)表于 2025-3-26 04:11:36 | 只看該作者
27#
發(fā)表于 2025-3-26 05:47:53 | 只看該作者
Nephrogenic Diabetes Insipidus and Vasopressin Receptor Mutations,jor action of AVP is to facilitate urinary concentration by allowing water to be transported passively down an osmotic gradient between the tubular fluid and the surrounding interstitium. The process of this counter multiplication system and the action of AVP on principal collecting duct cells are represented in Fig. 1.
28#
發(fā)表于 2025-3-26 09:08:01 | 只看該作者
https://doi.org/10.1007/978-3-658-05955-2t hypercal-cemia, is caused by activating mutations in the parathyroid hormone (PTH) PTH-related peptide (PTHrP) receptor. These findings are likely to have significant implications for understanding the biological importance of the PTH/PTHrP receptor in addition to its role in regulating mineral ion homeostasis.
29#
發(fā)表于 2025-3-26 15:17:24 | 只看該作者
,Constitutively Active PTH/PTHrP Receptors Cause Jansen’s Metaphyseal Chondrodysplasia,t hypercal-cemia, is caused by activating mutations in the parathyroid hormone (PTH) PTH-related peptide (PTHrP) receptor. These findings are likely to have significant implications for understanding the biological importance of the PTH/PTHrP receptor in addition to its role in regulating mineral ion homeostasis.
30#
發(fā)表于 2025-3-26 17:23:22 | 只看該作者
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