Carbonic anhydrase III protects osteocytes from oxidative stress-Reference-Cited by-同舟云学术

Carbonic anhydrase III protects osteocytes from oxidative stress

Published:2017-09-19 Issue:1 Volume:32 Page:440-452
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Shi Chao¹²,Uda Yuhei²,Dedic Christopher²³,Azab Ehab²,Sun Ningyuan²,Hussein Amira I.⁴,Petty Christopher A.²,Fulzele Keertik²,Mitterberger‐Vogt Maria C.⁵,Zwerschke Werner⁵,Pereira Renata⁶,Wang Kunzheng¹,Pajevic Paola Divieti²

Affiliation:

1. Department of OrthopaedicsThe Second Affiliated Hospital of Xi'an Jiaotong University Xi'an China

2. Molecular and Cell BiologyHenry M. Goldman School of Dental Medicine Boston Massachusetts USA

3. Merks Laboratories Boston MA USA

4. Department of OrthopedicsSchool of Medicine, Boston University Boston Massachusetts USA

5. Cell Metabolism and Differentiation Research GroupUniversity of Innsbruck Innsbruck Austria

6. David Geffen School of MedicineUniversity of California, Los Angeles Los Angeles California USA

Funder

National Institute of Arthritis and Musculoskeletal and Skin Diseases

National Institute of Diabetes and Digestive and Kidney Diseases

Boston University

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.201700485rr

Reference45 articles.

1. Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST)

2. Identification of a 52 kb deletion downstream of the SOST gene in patients with van Buchem disease

3. Bone Dysplasia Sclerosteosis Results from Loss of the SOST Gene Product, a Novel Cystine Knot–Containing Protein

4. A Known SOST Gene Mutation Causes Sclerosteosis in a Familial and an Isolated Case from Brazilian Origin

5. SOST/sclerostin, an osteocyte-derived negative regulator of bone formation

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