Increased osteopontin contributes to inhibition of bone mineralization in FGF23-deficient mice.
PubMed Identifier: 24038141
author list: Yuan Q, Jiang Y, Zhao X, Sato T, Densmore M, Sch?ler C, Erben RG, McKee MD, Lanske B
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published in: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
has major subject area list: Calcification, Physiologic; Fibroblast Growth Factors; Osteopontin
has minor subject area list: Animals; Fibroblast Growth Factor-23; Hyperphosphatemia; In Situ Hybridization; Mice; Mice, Knockout; Real-Time Polymerase Chain Reaction
information resource reference: Yuan Q, Jiang Y, Zhao X, Sato T, Densmore M, Sch?ler C, Erben RG, McKee MD, Lanske B. Increased osteopontin contributes to inhibition of bone mineralization in FGF23-deficient mice. J Bone Miner Res. 2014 Mar; 29(3):693-704.
journal title abbreviation: J Bone Miner Res
publication date: 2014-03-01T00:00:00
year: 2014
type: Academic Article
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has subject area: Calcification, Physiologic
has subject area: Fibroblast Growth Factors
has subject area: Osteopontin
has subject area: Animals
has subject area: Hyperphosphatemia
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has subject area: Mice
has subject area: Mice, Knockout
has subject area: Real-Time Polymerase Chain Reaction
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Sato, Tadatoshi
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Post Docs: Post Doc - Open Rank Job Number: 2025-48103 Category: Research Location: Worcester, MA Shift: Day Exempt/Non-Exempt: Exempt Business Unit: UMass Chan Medical School Department: School - Rheumatology - W710085 Job Type: Full-Time Salary Grade: 86 Union Code: Non Union Position-W63-Residents/Post Docs Num. Openings: 1 Post Date: May 26, 2025 https://www.ummsjobs.com/job/11019/ The Sato Lab at UMass Med is seeking an enthusiastic postdoctoral fellow to join our team at the forefront of gene editing and cell therapy research. Our research group is focusing on elucidating the molecular mechanisms underlying rare diseases and autoimmune disorders. Through innovative approaches such as gene editing and cell therapy, we aim to develop novel therapeutic strategies to combat these conditions and improve patient outcomes. Project Highlights: Utilize CRISPR gene editing techniques Engineer and explore gene/cell therapies for disease treatment Investigate the genetic basis of rare skeletal and connective tissue diseases Unravel mechanisms underlying autoimmune disorders Interested candidates should submit a CV or resume, a cover letter with a short description outlining research interests and relevant experience, and contact information for three references to tadatoshi.sato@umassmed.edu. Please indicate the position you are applying for in the subject line.
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linked information resource: Increased osteopontin contributes to inhibition of bone mineralization in FGF23-deficient mice.

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