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Tmem16f-deficient mice

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Antigen/Gene or Protein Targets Anoctamin6/Tmem16F (Ano6)
Disease Keywords Osteoporosis
Relevance 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.
Production Details 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.
Conditional No
Zygosity Homozygous
Research Area Developmental Biology, Genetic Studies Tools, Structural Biology

References: 1 entry

Ehlen et al. 2013. J Bone Miner Res. 28(2):246-59. PMID: 22936354.


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References: 1 entry

Ehlen et al. 2013. J Bone Miner Res. 28(2):246-59. PMID: 22936354.


Add a reference

References: 1 entry

Ehlen et al. 2013. J Bone Miner Res. 28(2):246-59. PMID: 22936354.


Add a reference


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