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Tmem16f-deficient mice - A model for studying osteoporosis



Ref.-Nr. 3481

During vertebrate skeletal development, osteoblasts produce a mineralized bone matrix by deposition of hydroxyapatite crystals in the extracellular matrix. Anoctamin6/Tmem16F (Ano6) belongs to a conserved family of transmembrane proteins. The gene Ano6 encodes a Ca-activated chloride channel. In addition, Ano6 has been linked to phosphatidylserine (PS) scrambling in the plasma membrane. During skeletogenesis, Ano6 mRNA is expressed in differentiating and mature osteoblasts.


Tmem16f-deficient mice were generated by complete gene deletion.
Deletion of Ano6 in mice results in reduced skeleton size and skeletal deformities. 
However, analysis of endochondral ossification on the molecular level reveals that proliferation and differentiation of chondrocytes is not affected, whereas the ossification process is significantly delayed. The transgenic mice display increased regions of nonmineralized, Ibsp-expressing osteoblasts in the periosteum during embryonic development and increased areas of uncalcified osteoid postnatally. 
Furthermore, calcium-dependent phospholipid scrambling is impaired in Tmem16f-defcient osteoblasts, supporting a function of PS exposure in the deposition of hydroxyapatite.

Keywords: Maus, mouse, Mausmodell, mouse model, complete gene deletion, Forschungstool, research tool, Osteoporose, osteoporosis, Skelettentwicklung, skeletal development, ossification, TMEM16F, Ano6, Anoctamin-6, Kalzium aktivierter Chlorid-Kanal, Ca activated chlorid channel

Current Status  

On behalf of the University of Duisburg-Essen, PROvendis offers access to the mouse model under a Material License Agreement.

Relevant Publication

H.W. Ehlen et al. (2013): Inactivation of anoctamin-6/Tmem16f, a regulator of phosphatidylserine scrambling in osteoblasts, leads to decreased mineral deposition in skeletal tissues. J Bone Miner Res. 2013 Feb; 28 (2):246-59.

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Dr. Jürgen Walkenhorst
+49.208 94105-25

Dr. Jürgen Walkenhorst

Dieses Angebot


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