Expression patterns of the Tmem16 gene family during cephalic development in the mouse

Gritli-Linde, Amel; Sani, Forugh Vaziri; Rock, Jason R.; Hallberg, K.; Iribarne, Daniela; Harfe, Brian D.; Linde, Anders

doi:10.1016/j.gep.2008.11.002

Cited by 34 publications

(31 citation statements)

References 24 publications

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“…1). (11,13,15) In the current study, we have characterized the role of Ano6 during differentiation and mineralization of the mouse skeleton. Analysis of wild-type and Ano6 À/À mice revealed that Ano6 is expressed at early osteoblast differentiation stages.…”

Section: Ano6mentioning

confidence: 99%

“…With vascular invasion, osteoblasts and osteoclasts enter the cartilage anlagen and start to replace hypertrophic cartilage with trabecular bone and bone marrow. In mice and human, Anoctamins form a family of 10 multitransmembrane proteins that show distinct but overlapping expression patterns in a variety of tissues and cell types during development (11)(12)(13)(14)(15) (reviewed in Flores and colleagues (16) and Galietta (17) ). Recently, Anoctamin1/Tmem16A (Ano1) has been identified as a calcium-activated chloride channel acting in several tissues and cell lines.…”

Section: Introductionmentioning

confidence: 99%

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Inactivation of anoctamin-6/Tmem16f, a regulator of phosphatidylserine scrambling in osteoblasts, leads to decreased mineral deposition in skeletal tissues

Ehlen

Chinenkova

Moser

et al. 2012

Journal of Bone and Mineral Research

114

106

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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 with chloride channel properties. 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. Deletion of Ano6 in mice results in reduced skeleton size and skeletal deformities. Molecular analysis revealed that chondrocyte and osteoblast differentiation are not disturbed. However, mutant mice display increased regions of nonmineralized, Ibsp-expressing osteoblasts in the periosteum during embryonic development and increased areas of uncalcified osteoid postnatally. In primary Ano6 À/À osteoblasts, mineralization is delayed, indicating a cell autonomous function of Ano6. Furthermore, we demonstrate that calcium-dependent PS scrambling is impaired in osteoblasts. Our study is the first to our knowledge to reveal the requirement of Ano6 in PS scrambling in osteoblasts, supporting a function of PS exposure in the deposition of hydroxyapatite. ß

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Section: Ano6mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inactivation of anoctamin-6/Tmem16f, a regulator of phosphatidylserine scrambling in osteoblasts, leads to decreased mineral deposition in skeletal tissues

Ehlen

Chinenkova

Moser

et al. 2012

Journal of Bone and Mineral Research

114

106

View full text Add to dashboard Cite

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“…The knockout mouse for TMEM16A was generated after the observation of TMEM16A enrichment in the zone of polarizing activity at the distal limb, before molecular identification of TMEM16A as CaCC (Rock et al, 2008). These mice have been used to validate TMEM16A expression and func-4 tion by immunocytochemistry, biophysical and physiological studies (Flores et al, 2009;Galietta, 2009;Gomez-Pinilla et al, 2009;Gritli-Linde et al, 2009;Huang et al, 2009;Hwang et al, 2009;Rock et al, 2009).…”

Section: Expression and Physiological Function Of Transmembrane mentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. LXXXV: Calcium-Activated Chloride Channels

Huang¹,

Wong²,

Jan³

2011

Pharmacol Rev

159

139

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“…This view was later changed. Recent studies identified both TMEM16A and TMEM16B in VSMCs [89,154,213,214,215]. The expression level of TMEM16B in VSMCs was relatively low in comparison with TMEM16A, which has a specific expression-density pattern over different vascular beds.…”

Section: Tmem16a and Tmem16b The Putative ‘Classical’ Caccmentioning

confidence: 99%

“…Other members of the TMEM16 protein family were also found in VSMCs: TMEM16F and TMEM16K were especially abundant while a weak expression of TMEM16D and TMEM16E was also detected [214,215]. However, TMEM16F and TMEM16K are ubiquitously expressed in different tissues and even in cells which do not express native I Cl(Ca) , suggesting that these proteins may have another function [23].…”

Section: Tmem16a and Tmem16b The Putative ‘Classical’ Caccmentioning

confidence: 99%

Transport and Function of Chloride in Vascular Smooth Muscles

et al. 2012

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This review summarizes the current knowledge of Cl^– transport in vascular smooth muscle cells (VSMCs). VSMCs accumulate Cl^– intracellularly using two secondary-active transport mechanisms. The Cl^– equilibrium potential is more positive than the resting membrane potential enabling Cl^– to be a depolarizing ion upon activation of a Cl^– conductance. Cl^– currents are involved in different vascular responses suggesting a number of different Cl^– channels. All known Cl^– channel families, with the exception of the GABA-/glycine-receptor family, have been identified in VSMCs. At least one member of the voltage-activated ClC family – ClC-3 – has been suggested to be involved in myogenic constriction, in cell proliferation and to have an anti-apoptotic action. The cystic fibrosis transmembrane conductance regulator is also demonstrated in VSMCs. The molecular identity of the major anion conductance in VSMCs – a Ca²⁺-activated Cl^– current – is uncertain. Several candidates have been suggested with bestrophin and TMEM16 protein families the current favorites. Specific pharmacological tools are lacking for Cl^– channels but recent molecular biology developments have made selective gene manipulations possible. A continuing quest within the vascular research field is to explicitly demonstrate the coupling between a putative channel protein and an endogenous Cl^– current and the importance of these for specific functions.

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Expression patterns of the Tmem16 gene family during cephalic development in the mouse

Cited by 34 publications

References 24 publications

Inactivation of anoctamin-6/Tmem16f, a regulator of phosphatidylserine scrambling in osteoblasts, leads to decreased mineral deposition in skeletal tissues

Inactivation of anoctamin-6/Tmem16f, a regulator of phosphatidylserine scrambling in osteoblasts, leads to decreased mineral deposition in skeletal tissues

International Union of Basic and Clinical Pharmacology. LXXXV: Calcium-Activated Chloride Channels

Transport and Function of Chloride in Vascular Smooth Muscles

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