Deletion of PTH rescues skeletal abnormalities and high osteopontin levels in Klotho-/- mice (Q27333726)

1

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Tadatoshi Sato

2

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Michael Densmore

3

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Hiroaki Saito

4

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Christiane Schüler

5

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Beate Lanske

Creative Commons Attribution 4.0 International

7

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language of work or name

English

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publication date

2012

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published in

PLOS Genetics

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volume

8

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issue

5

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page(s)

e1002726

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copyright license

start time

17 May 2012

1 reference

April 2022 Public Data File from Crossref

copyright status

copyrighted

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cites work

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FGF-23/Klotho signaling is not essential for the phosphaturic and anabolic functions of PTH.

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Inactivation of klotho function induces hyperphosphatemia even in presence of high serum fibroblast growth factor 23 levels in a genetically engineered hypophosphatemic (Hyp) mouse model

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The beta-glucuronidase klotho hydrolyzes and activates the TRPV5 channel

28 September 2017

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Regulation of matrix Gla protein by parathyroid hormone in MC3T3-E1 osteoblast-like cells involves protein kinase A and extracellular signal-regulated kinase pathways

28 September 2017

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Crossref

https://api.crossref.org/works/10.1371%2FJOURNAL.PGEN.1002726

FGF-23 transgenic mice demonstrate hypophosphatemic rickets with reduced expression of sodium phosphate cotransporter type IIa.

21 January 2018

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https://api.crossref.org/works/10.1371%2FJOURNAL.PGEN.1002726

Fibroblast growth factor-23 regulates parathyroid hormone and 1alpha-hydroxylase expression in cultured bovine parathyroid cells

21 January 2018

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https://api.crossref.org/works/10.1371%2FJOURNAL.PGEN.1002726

Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process

21 January 2018

1 reference

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Skeletal abnormalities in Pth-null mice are influenced by dietary calcium

27 November 2018

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/22615584

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Type I membrane klotho expression is decreased and inversely correlated to serum calcium in primary hyperparathyroidism

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/22615584

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Identifiers

DOI

10.1371/JOURNAL.PGEN.1002726

1 reference

1 reference

1 reference

PubMed publication ID

22615584

1 reference