ArticleThe Journal of clinical investigation2009
The peptidyl-prolyl isomerase Pin1 determines parathyroid hormone mRNA levels and stability in rat models of secondary hyperparathyroidism.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 94 citations in OpenAlex.
- Proline-directed phosphorylation and prolyl isomerization oppose each other to regulate PSD-95 ubiquitination and excitatory synaptic plasticity.Frontiers in molecular neuroscience · 2026Article
- Severe Hypocalcemia During JAK1/2 Inhibitor Therapy for Myelofibrosis in a Patient with Liver Cirrhosis.Internal medicine (Tokyo, Japan) · 2025Article
- The roles of mTORC1 in parathyroid gland function in chronic kidney disease-induced secondary hyperparathyroidism: Evidence from male genetic mouse models and clinical data.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- K-Homology Type Splicing Regulatory Protein: Mechanism of Action in Cancer and Immune Disorders.Critical reviews in eukaryotic gene expression · 2024Article
- The molecular mechanisms of peptidyl-prolylFrontiers in pharmacology · 2024Review
- Frontiers in Bone Metabolism and Disorder in Chronic Kidney Disease.Metabolites · 2023Article
- Article
- A Molecular Insight of the Role of PIN-1 Promoter Polymorphism (- 667C > T; rs2233679) in Chronic Kidney Disease Patients with Secondary Hyperparathyroidism.Indian journal of clinical biochemistry : IJCB · 2022Article
- Molecular Mechanisms of Parathyroid Disorders in Chronic Kidney Disease.Metabolites · 2022Review
- mRNA Profiles of Porcine Parathyroid Glands Following Variable Phosphorus Supplies throughout Fetal and Postnatal Life.Biomedicines · 2021Article
- Phosphate as a Signaling Molecule.Calcified tissue international · 2021Review
- Post-translational Control of RNA-Binding Proteins and Disease-Related Dysregulation.Frontiers in molecular biosciences · 2021Review
- Parathyroid Cell Proliferation in Secondary Hyperparathyroidism of Chronic Kidney Disease.International journal of molecular sciences · 2020Review
- Potential Anti-Tumor Activity of Kefir-Induced Juglone and Resveratrol Fractions Against Ehrlich Ascites Carcinoma-Bearing BALB/C Mice.Iranian journal of pharmaceutical research : IJPR · 2020Article
- Pinning Down the Transcription: A Role for Peptidyl-ProlylFrontiers in cell and developmental biology · 2020Review
- Juglone in Oxidative Stress and Cell Signaling.Antioxidants (Basel, Switzerland) · 2019Review
- Oncogenic Hijacking of the PIN1 Signaling Network.Frontiers in oncology · 2019Review
- Pin1 and secondary hyperparathyroidism of chronic kidney disease: gene polymorphisms and protein levels.Renal failure · 2017Article
- Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary hyperparathyroidism is a major complication of chronic kidney disease (CKD). In experimental models of secondary hyperparathyroidism induced by hypocalcemia or CKD, parathyroid hormone (PTH) mRNA levels increase due to increased PTH mRNA stability. K-homology splicing regulator protein (KSRP) decreases the stability of PTH mRNA upon binding a cis-acting element in the PTH mRNA 3' UTR region. As the peptidyl-prolyl isomerase (PPIase) Pin1 has recently been shown to regulate the turnover of multiple cytokine mRNAs, we investigated the role of Pin1 in regulating PTH mRNA stability in rat parathyroids and transfected cells. The data generated were consistent with Pin1 being a PTH mRNA destabilizing protein. Initial analysis indicated that Pin1 activity was decreased in parathyroid protein extracts from both hypocalcemic and CKD rats and that pharmacologic inhibition of Pin1 increased PTH mRNA levels posttranscriptionally in rat parathyroid and in transfected cells. Pin1 mediated its effects via interaction with KSRP, which led to KSRP dephosphorylation and activation. In the rat parathyroid, Pin1 inhibition decreased KSRP-PTH mRNA interactions, increasing PTH mRNA levels. Furthermore, Pin1-/- mice displayed increased serum PTH and PTH mRNA levels, suggesting that Pin1 determines basal PTH expression in vivo. These results demonstrate that Pin1 is a key mediator of PTH mRNA stability and indicate a role for Pin1 in the pathogenesis of secondary hyperparathyroidism in individuals with CKD.
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