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Journal articles on the topic 'Tmem30a'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Yang, Yeming, Wenjing Liu, Kuanxiang Sun, Li Jiang, and Xianjun Zhu. "Tmem30a deficiency leads to retinal rod bipolar cell degeneration." Journal of Neurochemistry 148, no. 3 (2019): 400–412. http://dx.doi.org/10.1111/jnc.14643.

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Zhang, Shanshan, Wenjing Liu, Yeming Yang, et al. "TMEM30A deficiency in endothelial cells impairs cell proliferation and angiogenesis." Journal of Cell Science 132, no. 7 (2019): jcs225052. http://dx.doi.org/10.1242/jcs.225052.

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3

Chen, Rui, Erin Brady, and Thomas M. McIntyre. "Human TMEM30a Promotes Uptake of Antitumor and Bioactive Choline Phospholipids into Mammalian Cells." Journal of Immunology 186, no. 5 (2011): 3215–25. http://dx.doi.org/10.4049/jimmunol.1002710.

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4

Yang, Fan, Yumin Huang, Xianda Chen, et al. "Deletion of a flippase subunit Tmem30a in hematopoietic cells impairs mouse fetal liver erythropoiesis." Haematologica 104, no. 10 (2019): 1984–94. http://dx.doi.org/10.3324/haematol.2018.203992.

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Wang, Jiao, Qian Wang, Dongfang Lu, et al. "A biosystems approach to identify the molecular signaling mechanisms of TMEM30A during tumor migration." PLOS ONE 12, no. 6 (2017): e0179900. http://dx.doi.org/10.1371/journal.pone.0179900.

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Yang, Yeming, Kuanxiang Sun, Wenjing Liu та ін. "The phosphatidylserine flippase β-subunit Tmem30a is essential for normal insulin maturation and secretion". Molecular Therapy 29, № 9 (2021): 2854–72. http://dx.doi.org/10.1016/j.ymthe.2021.04.026.

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7

Liu, Leiming, Lingling Zhang, Lin Zhang, et al. "Hepatic Tmem30a Deficiency Causes Intrahepatic Cholestasis by Impairing Expression and Localization of Bile Salt Transporters." American Journal of Pathology 187, no. 12 (2017): 2775–87. http://dx.doi.org/10.1016/j.ajpath.2017.08.011.

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8

Ennishi, Daisuke, Shannon Healy, Ali Bashashati, et al. "TMEM30A loss-of-function mutations drive lymphomagenesis and confer therapeutically exploitable vulnerability in B-cell lymphoma." Nature Medicine 26, no. 4 (2020): 577–88. http://dx.doi.org/10.1038/s41591-020-0757-z.

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9

Li, Ning, Yeming Yang, Cailing Liang, et al. "Tmem30a Plays Critical Roles in Ensuring the Survival of Hematopoietic Cells and Leukemia Cells in Mice." American Journal of Pathology 188, no. 6 (2018): 1457–68. http://dx.doi.org/10.1016/j.ajpath.2018.02.015.

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10

Sun, Kuanxiang, Wanli Tian, Xiao Li, Wenjing Liu, Yeming Yang, and Xianjun Zhu. "Disease Mutation Study Identifies Critical Residues for Phosphatidylserine Flippase ATP11A." BioMed Research International 2020 (June 2, 2020): 1–9. http://dx.doi.org/10.1155/2020/7342817.

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Phosphatidylserine flippase (P4-ATPase) transports PS from the outer to the inner leaflet of the lipid bilayer in the membrane to maintain PS asymmetry, which is important for biological activities of the cell. ATP11A is expressed in multiple tissues and plays a role in myotube formation. However, the detailed cellular function of ATP11A remains elusive. Mutation analysis revealed that I91, L308, and E897 residues in ATP8A2 are important for flippase activity. In order to investigate the roles of these corresponding amino acid residues in ATP11A protein, we assessed the expression and cellular

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Luo, Shuo, Xin Wang, Meirong Bai, et al. "The conserved autoimmune-disease risk gene TMEM39A regulates lysosome dynamics." Proceedings of the National Academy of Sciences 118, no. 6 (2021): e2011379118. http://dx.doi.org/10.1073/pnas.2011379118.

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TMEM39A encodes an evolutionarily conserved transmembrane protein and carries single-nucleotide polymorphisms associated with increased risk of major human autoimmune diseases, including multiple sclerosis. The exact cellular function of TMEM39A remains not well understood. Here, we report that TMEM-39, the sole Caenorhabditis elegans (C. elegans) ortholog of TMEM39A, regulates lysosome distribution and accumulation. Elimination of tmem-39 leads to lysosome tubularization and reduced lysosome mobility, as well as accumulation of the lysosome-associated membrane protein LMP-1. In mammalian cell

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Sun, Kuan-Xiang, Xiao-Yan Jiang, Xiao Li та ін. "Deletion of phosphatidylserine flippase β-subunit Tmem30a in satellite cells leads to delayed skeletal muscle regeneration". Zoological Research 42, № 5 (2021): 650–59. http://dx.doi.org/10.24272/j.issn.2095-8137.2021.195.

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Takasugi, Nobumasa, Runa Araya, Yuji Kamikubo та ін. "TMEM30A is a candidate interacting partner for the β-carboxyl-terminal fragment of amyloid-β precursor protein in endosomes". PLOS ONE 13, № 8 (2018): e0200988. http://dx.doi.org/10.1371/journal.pone.0200988.

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14

Zhou, Xinyu, Ang Li, Pei-hui Lin, Jingsong Zhou, and Jianjie Ma. "TRIC-A regulates intracellular Ca2+ homeostasis in cardiomyocytes." Pflügers Archiv - European Journal of Physiology 473, no. 3 (2021): 547–56. http://dx.doi.org/10.1007/s00424-021-02513-6.

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AbstractTrimeric intracellular cation (TRIC) channels have been identified as monovalent cation channels that are located in the ER/SR membrane. Two isoforms discovered in mammals are TRIC-A (TMEM38a) and TRIC-B (TMEM38b). TRIC-B ubiquitously expresses in all tissues, and TRIC-B−/− mice is lethal at the neonatal stage. TRIC-A mainly expresses in excitable cells. TRIC-A−/− mice survive normally but show abnormal SR Ca2+ handling in both skeletal and cardiac muscle cells. Importantly, TRIC-A mutations have been identified in human patients with stress-induced arrhythmia. In the past decade, impo

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15

Zhang, Zhe, Shuo Luo, Guilherme Oliveira Barbosa, Meirong Bai, Thomas B. Kornberg, and Dengke K. Ma. "The conserved transmembrane protein TMEM-39 coordinates with COPII to promote collagen secretion and regulate ER stress response." PLOS Genetics 17, no. 2 (2021): e1009317. http://dx.doi.org/10.1371/journal.pgen.1009317.

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Dysregulation of collagen production and secretion contributes to aging and tissue fibrosis of major organs. How procollagen proteins in the endoplasmic reticulum (ER) route as specialized cargos for secretion remains to be fully elucidated. Here, we report that TMEM39, an ER-localized transmembrane protein, regulates production and secretory cargo trafficking of procollagen. We identify the C. elegans ortholog TMEM-39 from an unbiased RNAi screen and show that deficiency of tmem-39 leads to striking defects in cuticle collagen production and constitutively high ER stress response. RNAi knockd

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16

Wang, Xiaobo, Gongbo Guo, Jinru Zhang, et al. "Mutant-TMEM230-induced neurodegeneration and impaired axonal mitochondrial transport." Human Molecular Genetics 30, no. 16 (2021): 1535–42. http://dx.doi.org/10.1093/hmg/ddab128.

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Abstract Parkinson’s disease (PD) is a neurodegenerative disease with movement disorders including resting tremor, rigidity, bradykinesia and postural instability. Recent studies have identified a new PD associated gene, TMEM230 (transmembrane protein 230). However, the pathological roles of TMEM230 and its variants are not fully understood. TMEM230 gene encodes two protein isoforms. Isoform2 is the major protein form (~95%) in human. In this study, we overexpress isoform2 TMEM230 variants (WT or PD-linked *184Wext*5 mutant) or knockdown endogenous protein in cultured SH-5Y5Y cells and mouse p

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Talbi, Khaoula, Jiraporn Ousingsawat, Raquel Centeio, Rainer Schreiber, and Karl Kunzelmann. "Calmodulin-Dependent Regulation of Overexpressed but Not Endogenous TMEM16A Expressed in Airway Epithelial Cells." Membranes 11, no. 9 (2021): 723. http://dx.doi.org/10.3390/membranes11090723.

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Regulation of the Ca2+-activated Cl− channel TMEM16A by Ca2+/calmodulin (CAM) is discussed controversially. In the present study, we compared regulation of TMEM16A by Ca2+/calmodulin (holo-CAM), CAM-dependent kinase (CAMKII), and CAM-dependent phosphatase calcineurin in TMEM16A-overexpressing HEK293 cells and TMEM16A expressed endogenously in airway and colonic epithelial cells. The activator of the Ca2+/CAM-regulated K+ channel KCNN4, 1-EBIO, activated TMEM16A in overexpressing cells, but not in cells with endogenous expression of TMEM16A. Evidence is provided that CAM-interaction with TMEM16

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Zhuang, Jinfu, Yongjian Huang, Wei Zheng, et al. "TMEM100 expression suppresses metastasis and enhances sensitivity to chemotherapy in gastric cancer." Biological Chemistry 401, no. 2 (2020): 285–96. http://dx.doi.org/10.1515/hsz-2019-0161.

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AbstractThe gene encoding transmembrane protein 100 (TMEM100) was first discovered to be transcribed by the murine genome. It has been recently proven that TMEM100 contributes to hepatocellular carcinoma and non-small-cell lung carcinoma (NSCLC). This study investigates the impact of TMEM100 expression on gastric cancer (GC). TMEM100 expression was remarkably downregulated in GC samples compared to the surrounding non-malignant tissues (p < 0.01). Excessive TMEM100 expression prohibited the migration and invasion of GC cells without influencing their growth. However, TMEM100 knockdown resto

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19

Simões, Filipa B., Margarida C. Quaresma, Luka A. Clarke, et al. "TMEM16A chloride channel does not drive mucus production." Life Science Alliance 2, no. 6 (2019): e201900462. http://dx.doi.org/10.26508/lsa.201900462.

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Airway mucus obstruction is the main cause of morbidity in cystic fibrosis, a disease caused by mutations in the CFTR Cl− channel. Activation of non-CFTR Cl− channels such as TMEM16A can likely compensate for defective CFTR. However, TMEM16A was recently described as a key driver in mucus production/secretion. Here, we have examined whether indeed there is a causal relationship between TMEM16A and MUC5AC production, the main component of respiratory mucus. Our data show that TMEM16A and MUC5AC are inversely correlated during differentiation of human airway cells. Furthermore, we show for the f

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20

Centeio, Raquel, Inês Cabrita, Roberta Benedetto, et al. "Pharmacological Inhibition and Activation of the Ca2+ Activated Cl− Channel TMEM16A." International Journal of Molecular Sciences 21, no. 7 (2020): 2557. http://dx.doi.org/10.3390/ijms21072557.

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TMEM16A is a Ca2+ activated Cl− channel with important functions in airways, intestine, and other epithelial organs. Activation of TMEM16A is proposed as a therapy in cystic fibrosis (CF) to reinstall airway Cl− secretion and to enhance airway surface liquid (ASL). This CFTR-agnostic approach is thought to improve mucociliary clearance and lung function in CF. This could indeed improve ASL, however, mucus release and airway contraction may also be induced by activators of TMEM16A, particularly in inflamed airways of patients with asthma, COPD, or CF. Currently, both activators and inhibitors o

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21

Li, Huixia, Chuan Cheng, Weibo You та ін. "TMEM100 Modulates TGF-β Signaling Pathway to Inhibit Colorectal Cancer Progression". Gastroenterology Research and Practice 2021 (11 серпня 2021): 1–10. http://dx.doi.org/10.1155/2021/5552324.

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Objectives. This study investigated the functional mechanism of transmembrane protein 100 (TMEM100) as a tumor inhibitor gene in CRC cells and offered a reference for the treatment of CRC. Methods. The mRNA expression data of CRC were acquired from the TCGA database to mine differentially expressed mRNAs. The role of TMEM100 in the progression of CRC cells was evaluated by MTT, colony formation, scratch healing, and Transwell assays. The influence of TMEM100 on the TGF-β signaling pathway was detected by western blot. Results. TMEM100 was markedly lowly expressed in CRC. CRC cell growth was si

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22

Danielsson, Jennifer, Aisha S. Kuforiji, Gene T. Yocum, et al. "Agonism of the TMEM16A calcium-activated chloride channel modulates airway smooth muscle tone." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 2 (2020): L287—L295. http://dx.doi.org/10.1152/ajplung.00552.2018.

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TMEM16A (anoctamin 1) is an important calcium-activated chloride channel in airway smooth muscle (ASM). We have previously shown that TMEM16A antagonists such as benzbromarone relax ASM and have proposed TMEM16A antagonists as novel therapies for asthma treatment. However, TMEM16A is also expressed on airway epithelium, and TMEM16A agonists are being investigated as novel therapies for cystic fibrosis. There are theoretical concerns that agonism of TMEM16A on ASM could lead to bronchospasm, making them detrimental as airway therapeutics. The TMEM16A agonist Eact induced a significant contracti

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23

Catalán, Marcelo A., Yusuke Kondo, Gaspar Peña-Munzenmayer, et al. "A fluid secretion pathway unmasked by acinar-specific Tmem16A gene ablation in the adult mouse salivary gland." Proceedings of the National Academy of Sciences 112, no. 7 (2015): 2263–68. http://dx.doi.org/10.1073/pnas.1415739112.

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Activation of an apical Ca2+-activated Cl− channel (CaCC) triggers the secretion of saliva. It was previously demonstrated that CaCC-mediated Cl− current and Cl− efflux are absent in the acinar cells of systemic Tmem16A (Tmem16A Cl− channel) null mice, but salivation was not assessed in fully developed glands because Tmem16A null mice die within a few days after birth. To test the role of Tmem16A in adult salivary glands, we generated conditional knockout mice lacking Tmem16A in acinar cells (Tmem16A−/−). Ca2+-dependent salivation was abolished in Tmem16A−/− mice, demonstrating that Tmem16A is

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Pinto, Madalena C., Rainer Schreiber, Joana Lerias, et al. "Regulation of TMEM16A by CK2 and Its Role in Cellular Proliferation." Cells 9, no. 5 (2020): 1138. http://dx.doi.org/10.3390/cells9051138.

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Casein kinase 2 (CK2) is a highly ubiquitous and conserved serine/threonine kinase that forms a tetramer consisting of a catalytic subunit (CK2α) and a regulatory subunit (CK2β). Despite being ubiquitous, CK2 is commonly found at higher expression levels in cancer cells, where it inhibits apoptosis, and supports cell migration and proliferation. The Ca2+-activated chloride channel TMEM16A shows similar effects in cancer cells: TMEM16A increases cell proliferation and migration and is highly expressed in squamous cell carcinoma of the head and neck (HNSCC) as well as other malignant tumors. A m

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Centeio, Raquel, Jiraporn Ousingsawat, Inês Cabrita, et al. "Mucus Release and Airway Constriction by TMEM16A May Worsen Pathology in Inflammatory Lung Disease." International Journal of Molecular Sciences 22, no. 15 (2021): 7852. http://dx.doi.org/10.3390/ijms22157852.

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Activation of the Ca2+ activated Cl− channel TMEM16A is proposed as a treatment in inflammatory airway disease. It is assumed that activation of TMEM16A will induce electrolyte secretion, and thus reduce airway mucus plugging and improve mucociliary clearance. A benefit of activation of TMEM16A was shown in vitro and in studies in sheep, but others reported an increase in mucus production and airway contraction by activation of TMEM16A. We analyzed expression of TMEM16A in healthy and inflamed human and mouse airways and examined the consequences of activation or inhibition of TMEM16A in asthm

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Crottès, David, Yu-Hsiu T. Lin, Christian J. Peters, et al. "TMEM16A controls EGF-induced calcium signaling implicated in pancreatic cancer prognosis." Proceedings of the National Academy of Sciences 116, no. 26 (2019): 13026–35. http://dx.doi.org/10.1073/pnas.1900703116.

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Pancreatic cancer typically spreads rapidly and has poor survival rates. Here, we report that the calcium-activated chloride channel TMEM16A is a biomarker for pancreatic cancer with a poor prognosis. TMEM16A is up-regulated in 75% of cases of pancreatic cancer and high levels of TMEM16A expression are correlated with low patient survival probability. TMEM16A up-regulation is associated with the ligand-dependent EGFR signaling pathway. In vitro, TMEM16A is required for EGF-induced store-operated calcium entry essential for pancreatic cancer cell migration. TMEM16A also has a profound impact on

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Ko, Woori, and Byung-Chang Suh. "Differential Regulation of Ca2+-Activated Cl− Channel TMEM16A Splice Variants by Membrane PI(4,5)P2." International Journal of Molecular Sciences 22, no. 8 (2021): 4088. http://dx.doi.org/10.3390/ijms22084088.

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TMEM16A is a Ca2+-activated Cl− channel that controls broad cellular processes ranging from mucus secretion to signal transduction and neuronal excitability. Recent studies have reported that membrane phospholipid phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) is an important cofactor that allosterically regulates TMEM16A channel activity. However, the detailed regulatory actions of PIP2 in splice variants of TMEM16A remain unclear. Here, we demonstrated that the attenuation of membrane phosphoinositide levels selectively inhibited the current amplitude of the TMEM16A(ac) isoform by decreas

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Ehrlich, Kenneth C., Michelle Lacey, and Melanie Ehrlich. "Epigenetics of Skeletal Muscle-Associated Genes in the ASB, LRRC, TMEM, and OSBPL Gene Families." Epigenomes 4, no. 1 (2020): 1. http://dx.doi.org/10.3390/epigenomes4010001.

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Much remains to be discovered about the intersection of tissue-specific transcription control and the epigenetics of skeletal muscle (SkM), a very complex and dynamic organ. From four gene families, Leucine-Rich Repeat Containing (LRRC), Oxysterol Binding Protein Like (OSBPL), Ankyrin Repeat and Socs Box (ASB), and Transmembrane Protein (TMEM), we chose 21 genes that are preferentially expressed in human SkM relative to 52 other tissue types and analyzed relationships between their tissue-specific epigenetics and expression. We also compared their genetics, proteomics, and descriptions in the

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Leo, M. Dennis, Dieniffer Peixoto-Nieves, Wen Yin, et al. "TMEM16A channel upregulation in arterial smooth muscle cells produces vasoconstriction during diabetes." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 3 (2021): H1089—H1101. http://dx.doi.org/10.1152/ajpheart.00690.2020.

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We investigated the involvement of TMEM16A channels in vascular dysfunction during type 2 diabetes (T2D). TMEM16A message, protein, and currents were higher in smooth muscle cells of resistance-size arteries during T2D. Pressure stimulated greater vasoconstriction in the arteries of T2D mice that was abolished in the arteries of TMEM16A smKO mice. Akt2 protein and activity were both lower in T2D arteries, and Akt2 knockdown elevated TMEM16A protein. We propose that a decrease in Akt2 function stimulates TMEM16A expression in arterial smooth muscle cells, leading to vasoconstriction during T2D.

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Papp, Rita, Chandran Nagaraj, Diana Zabini, et al. "Targeting TMEM16A to reverse vasoconstriction and remodelling in idiopathic pulmonary arterial hypertension." European Respiratory Journal 53, no. 6 (2019): 1800965. http://dx.doi.org/10.1183/13993003.00965-2018.

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Our systematic analysis of anion channels and transporters in idiopathic pulmonary arterial hypertension (IPAH) showed marked upregulation of the Cl− channel TMEM16A gene. We hypothesised that TMEM16A overexpression might represent a novel vicious circle in the molecular pathways causing pulmonary arterial hypertension (PAH).We investigated healthy donor lungs (n=40) and recipient lungs with IPAH (n=38) for the expression of anion channel and transporter genes in small pulmonary arteries and pulmonary artery smooth muscle cells (PASMCs).In IPAH, TMEM16A was strongly upregulated and patch-clamp

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Dutta, Amal K., Al-Karim Khimji, Songling Liu та ін. "PKCα regulates TMEM16A-mediated Cl− secretion in human biliary cells". American Journal of Physiology-Gastrointestinal and Liver Physiology 310, № 1 (2016): G34—G42. http://dx.doi.org/10.1152/ajpgi.00146.2015.

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TMEM16A is a newly identified Ca2+-activated Cl− channel in biliary epithelial cells (BECs) that is important in biliary secretion. While extracellular ATP stimulates TMEM16A via binding P2 receptors and increasing intracellular Ca2+ concentration ([Ca2+]i), the regulatory pathways have not been elucidated. Protein kinase C (PKC) contributes to ATP-mediated secretion in BECs, although its potential role in TMEM16A regulation is unknown. To determine whether PKCα regulates the TMEM16A-dependent membrane Cl− transport in BECs, studies were performed in human biliary Mz-cha-1 cells. Addition of e

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Li, Yang, Sharmy J. James, David H. Wyllie, et al. "TMEM203 is a binding partner and regulator of STING-mediated inflammatory signaling in macrophages." Proceedings of the National Academy of Sciences 116, no. 33 (2019): 16479–88. http://dx.doi.org/10.1073/pnas.1901090116.

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Regulation of IFN signaling is critical in host recognition and response to pathogens while its dysregulation underlies the pathogenesis of several chronic diseases. STimulator of IFN Genes (STING) has been identified as a critical mediator of IFN inducing innate immune pathways, but little is known about direct coregulators of this protein. We report here that TMEM203, a conserved putative transmembrane protein, is an intracellular regulator of STING-mediated signaling. We show that TMEM203 interacts, functionally cooperates, and comigrates with STING following cell stimulation, which in turn

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Jiao, Hui-Feng, Xiang-Dong Sun, Ryan Bates, et al. "Transmembrane protein 108 is required for glutamatergic transmission in dentate gyrus." Proceedings of the National Academy of Sciences 114, no. 5 (2017): 1177–82. http://dx.doi.org/10.1073/pnas.1618213114.

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Neurotransmission in dentate gyrus (DG) is critical for spatial coding, learning memory, and emotion processing. Although DG dysfunction is implicated in psychiatric disorders, including schizophrenia, underlying pathological mechanisms remain unclear. Here we report that transmembrane protein 108 (Tmem108), a novel schizophrenia susceptibility gene, is highly enriched in DG granule neurons and its expression increased at the postnatal period critical for DG development. Tmem108 is specifically expressed in the nervous system and enriched in the postsynaptic density fraction. Tmem108-deficient

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Hao, Feng, Zhong Hai Yuan, Zhi Xin Wang, et al. "Plasmid Construction of TMEM16A-pcDNA3.1 and its Application to Transient and Stable Transfection of FRT Cells." Advanced Materials Research 554-556 (July 2012): 1734–37. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1734.

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Calcium-activated chloride channels (CaCCs) play pivotal roles in many physiological Activities, including transepithelial fluid secretion, smooth muscle contraction and sensory transduction. TMEM16A is a bona fide calcium-activated chloride channel，which was discovered by three independent labs in 2008 after Calcium-activated chloride channel current was recorded about thirty years ago. In this study, DNA fragments encoding mouse TMEM16A with green fluorescence protein (GFP) fusion protein were subcloned into pcDNA3.1/Zeo. Transient transfection condition was optimized and Fischer Thyroid epi

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Schreiber, Rainer, Björn Buchholz, Andre Kraus, et al. "Lipid Peroxidation Drives Renal Cyst Growth In Vitro through Activation of TMEM16A." Journal of the American Society of Nephrology 30, no. 2 (2019): 228–42. http://dx.doi.org/10.1681/asn.2018010039.

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BackgroundTransepithelial chloride− secretion, through the chloride channels cystic fibrosis transmembrane conductance regulator (CFTR) and TMEM16A (anoctamin 1), drives cyst enlargement in polycystic kidney disease (PKD). Polycystic kidneys are hypoxic, and oxidative stress activates TMEM16A. However, mechanisms for channel activation in PKD remain obscure.MethodsUsing tissue samples from patients with autosomal dominant PKD, embryonic kidney cultures, and an MDCK in vitro cyst model, we assessed peroxidation of plasma membrane phospholipids in human and mouse polycystic kidneys. We also used

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Thomas-Gatewood, Candice, Zachary P. Neeb, Simon Bulley, et al. "TMEM16A channels generate Ca2+-activated Cl− currents in cerebral artery smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (2011): H1819—H1827. http://dx.doi.org/10.1152/ajpheart.00404.2011.

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Transmembrane protein (TMEM)16A channels are recently discovered membrane proteins that display electrophysiological properties similar to classic Ca2+-activated Cl− (ClCa) channels in native cells. The molecular identity of proteins that generate ClCa currents in smooth muscle cells (SMCs) of resistance-size arteries is unclear. Similarly, whether cerebral artery SMCs generate ClCa currents is controversial. Here, using molecular biology and patch-clamp electrophysiology, we examined TMEM16A channel expression and characterized Cl− currents in arterial SMCs of resistance-size rat cerebral art

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Henriques, Tiago, Emilio Agostinelli, Andres Hernandez-Clavijo, et al. "TMEM16A calcium-activated chloride currents in supporting cells of the mouse olfactory epithelium." Journal of General Physiology 151, no. 7 (2019): 954–66. http://dx.doi.org/10.1085/jgp.201812310.

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Glial-like supporting (or sustentacular) cells are important constituents of the olfactory epithelium that are involved in several physiological processes such as production of endocannabinoids, insulin, and ATP and regulation of the ionic composition of the mucus layer that covers the apical surface of the olfactory epithelium. Supporting cells express metabotropic P2Y purinergic receptors that generate ATP-induced Ca2+ signaling through the activation of a PLC-mediated cascade. Recently, we reported that a subpopulation of supporting cells expresses also the Ca2+-activated Cl− channel TMEM16

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Centeio, Raquel, Jiraporn Ousingsawat, Rainer Schreiber, and Karl Kunzelmann. "CLCA1 Regulates Airway Mucus Production and Ion Secretion Through TMEM16A." International Journal of Molecular Sciences 22, no. 10 (2021): 5133. http://dx.doi.org/10.3390/ijms22105133.

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TMEM16A, a Ca2+-activated chloride channel (CaCC), and its regulator, CLCA1, are associated with inflammatory airway disease and goblet cell metaplasia. CLCA1 is a secreted protein with protease activity that was demonstrated to enhance membrane expression of TMEM16A. Expression of CLCA1 is particularly enhanced in goblet cell metaplasia and is associated with various lung diseases. However, mice lacking expression of CLCA1 showed the same degree of mucous cell metaplasia and airway hyperreactivity as asthmatic wild-type mice. To gain more insight into the role of CLCA1, we applied secreted N-

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Braggio, Esteban, Brian Patrick O'Neill, William Macon, Maria Beatriz Lopes, David Schiff, and Rafael Fonseca. "Characterization of the Copy-Number Changes In Primary CNS Lymphomas (PCNSL) by High-Resolution Array-Based Comparative Genomic Hybridization." Blood 116, no. 21 (2010): 995. http://dx.doi.org/10.1182/blood.v116.21.995.995.

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Abstract Abstract 995 PCNSL is an aggressive primary brain tumor characterized by a perivascular accumulation of malignant lymphoid cells. Most PCNSLs (90%) are diffuse large B-cell lymphoma (DLBCL); the remaining 10% are poorly characterized low-grade, Burkitt, and T-cell lymphomas. Since most patients are biopsed, genomic analyses are challenging. To determine the pattern of genetic alterations in PCNSL, frozen samples and formalin fixed embedded paraffin sections from 17 EBV and HIV negative and immunocompetent patients were studied by array-based comparative genomic hybridization (aCGH) us

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Cela, P., M. Hampl, N. A. Shylo, et al. "Ciliopathy Protein Tmem107 Plays Multiple Roles in Craniofacial Development." Journal of Dental Research 97, no. 1 (2017): 108–17. http://dx.doi.org/10.1177/0022034517732538.

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A broad spectrum of human diseases called ciliopathies is caused by defective primary cilia morphology or signal transduction. The primary cilium is a solitary organelle that responds to mechanical and chemical stimuli from extracellular and intracellular environments. Transmembrane protein 107 (TMEM107) is localized in the primary cilium and is enriched at the transition zone where it acts to regulate protein content of the cilium. Mutations in TMEM107 were previously connected with oral-facial-digital syndrome, Meckel-Gruber syndrome, and Joubert syndrome exhibiting a range of ciliopathic de

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Dutta, Amal K., Kristy Boggs, Al-karim Khimji, et al. "Signaling through the interleukin-4 and interleukin-13 receptor complexes regulates cholangiocyte TMEM16A expression and biliary secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 4 (2020): G763—G771. http://dx.doi.org/10.1152/ajpgi.00219.2019.

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TMEM16A is a Ca2+-activated Cl− channel in the apical membrane of biliary epithelial cells, known as cholangiocytes, which contributes importantly to ductular bile formation. Whereas cholangiocyte TMEM16A activity is regulated by extracellular ATP-binding membrane purinergic receptors, channel expression is regulated by interleukin-4 (IL-4) through an unknown mechanism. Therefore, the aim of the present study was to identify the signaling pathways involved in TMEM16A expression and cholangiocyte secretion. Studies were performed in polarized normal rat cholangiocyte monolayers, human Mz-Cha-1

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Ayon, Ramon J., Matthew B. Hawn, Joydeep Aoun, et al. "Molecular mechanism of TMEM16A regulation: role of CaMKII and PP1/PP2A." American Journal of Physiology-Cell Physiology 317, no. 6 (2019): C1093—C1106. http://dx.doi.org/10.1152/ajpcell.00059.2018.

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This study explored the mechanism by which Ca2+-activated Cl− channels (CaCCs) encoded by the Tmem16a gene are regulated by calmodulin-dependent protein kinase II (CaMKII) and protein phosphatases 1 (PP1) and 2A (PP2A). Ca2+-activated Cl− currents ( IClCa) were recorded from HEK-293 cells expressing mouse TMEM16A. IClCa were evoked using a pipette solution in which free Ca2+ concentration was clamped to 500 nM, in the presence (5 mM) or absence of ATP. With 5 mM ATP, IClCa decayed to <50% of the initial current magnitude within 10 min after seal rupture. IClCa rundown seen with ATP-containi

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Lu, Long-Feng, Can Zhang, Zhuo-Cong Li, et al. "A novel role of Zebrafish TMEM33 in negative regulation of interferon production by two distinct mechanisms." PLOS Pathogens 17, no. 2 (2021): e1009317. http://dx.doi.org/10.1371/journal.ppat.1009317.

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The transmembrane protein 33 (TMEM33) was originally identified as an endoplasmic reticulum (ER) protein that influences the tubular structure of the ER and modulates intracellular calcium homeostasis. However, the role of TMEM33 in antiviral immunity in vertebrates has not been elucidated. In this article, we demonstrate that zebrafish TMEM33 is a negative regulator of virus-triggered interferon (IFN) induction via two mechanisms: mitochondrial antiviral signaling protein (MAVS) ubiquitination and a decrease in the kinase activity of TANK binding kinase 1 (TBK1). Upon stimulation with viral c

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Schenk, Laura K., Bjoern Buchholz, Sebastian F. Henke, et al. "Nephron-specific knockout of TMEM16A leads to reduced number of glomeruli and albuminuria." American Journal of Physiology-Renal Physiology 315, no. 6 (2018): F1777—F1786. http://dx.doi.org/10.1152/ajprenal.00638.2017.

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TMEM16A is a transmembrane protein from a conserved family of calcium-activated proteins that is highly expressed in the kidney. TMEM16A confers calcium-activated chloride channel activity, which is of importance for various cellular functions in secretory epithelia and involved in secretion-dependent renal cyst growth. However, its specific function in renal physiology has remained elusive so far. Therefore, we generated conditional nephron-specific TMEM16A-knockout mice and found that these animals suffered from albuminuria. Kidney histology demonstrated an intact corticomedullary differenti

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Davis, Alison J., Abigail S. Forrest, Thomas A. Jepps, et al. "Expression profile and protein translation of TMEM16A in murine smooth muscle." American Journal of Physiology-Cell Physiology 299, no. 5 (2010): C948—C959. http://dx.doi.org/10.1152/ajpcell.00018.2010.

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Recently, overexpression of the genes TMEM16A and TMEM16B has been shown to produce currents qualitatively similar to native Ca2+-activated Cl− currents ( IClCa) in vascular smooth muscle. However, there is no information about this new gene family in vascular smooth muscle, where Cl− channels are a major depolarizing mechanism. Qualitatively similar Cl− currents were evoked by a pipette solution containing 500 nM Ca2+ in smooth muscle cells isolated from BALB/c mouse portal vein, thoracic aorta, and carotid artery. Quantitative PCR using SYBR Green chemistry and primers specific for transmemb

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Grigoriev, V. V. "Calcium-activated chloride channels: structure, properties, role in physiological and pathological processes." Biomeditsinskaya Khimiya 67, no. 1 (2021): 17–33. http://dx.doi.org/10.18097/pbmc20216701017.

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Ca2+-activated chloride channels (CaCC) are a class of intracellular calcium activated chloride channels that mediate numerous physiological functions. In 2008, the molecular structure of CaCC was determined. CaCC are formed by the protein known as anoctamine 1 (ANO1 or TMEM16A). CaCC mediates the secretion of Cl– in secretory epithelia, such as the airways, salivary glands, intestines, renal tubules, and sweat glands. The presence of CaCC has also been recognized in the vascular muscles, smooth muscles of the respiratory tract, which control vascular tone and hypersensitivity of the respirato

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Skofic Maurer, Davor, Diana Zabini, Chandran Nagaraj, et al. "Endothelial Dysfunction Following Enhanced TMEM16A Activity in Human Pulmonary Arteries." Cells 9, no. 9 (2020): 1984. http://dx.doi.org/10.3390/cells9091984.

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Endothelial dysfunction is one of the hallmarks of different vascular diseases, including pulmonary arterial hypertension (PAH). Ion channelome changes have long been connected to vascular remodeling in PAH, yet only recently has the focus shifted towards Ca2+-activated Cl− channels (CaCC). The most prominent member of the CaCC TMEM16A has been shown to contribute to the pathogenesis of idiopathic PAH (IPAH) in pulmonary arterial smooth muscle cells, however its role in the homeostasis of healthy human pulmonary arterial endothelial cells (PAECs) and in the development of endothelial dysfuncti

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Scudieri, Paolo, Elvira Sondo, Emanuela Caci, Roberto Ravazzolo, and Luis J. V. Galietta. "TMEM16A–TMEM16B chimaeras to investigate the structure–function relationship of calcium-activated chloride channels." Biochemical Journal 452, no. 3 (2013): 443–55. http://dx.doi.org/10.1042/bj20130348.

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TMEM16A and TMEM16B proteins are CaCCs (Ca2+-activated Cl− channels) with eight putative transmembrane segments. As shown previously, expression of TMEM16B generates CaCCs characterized by a 10-fold lower Ca2+ affinity and by faster activation and deactivation kinetics with respect to TMEM16A. To investigate the basis of the different properties, we generated chimaeric proteins in which different domains of the TMEM16A protein were replaced by the equivalent domains of TMEM16B. Replacement of the N-terminus, TMD (transmembrane domain) 1–2, the first intracellular loop and TMD3–4 did not change

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Hao, Feng, Yi Ju Hou, Chen Zhao, et al. "Expression Clone of TMEM16A as a Calcium-Activated Chloride Channels in CHO Cells." Advanced Materials Research 709 (June 2013): 832–35. http://dx.doi.org/10.4028/www.scientific.net/amr.709.832.

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There is compelling evidence that TMEM16A fuctions as calcium-activated chloride channels (CaCCS), which was discovered by three independent labs in 2008 after Calcium-activated chloride channel current was first recorded in the 1980s. CaCCs are involved in many physiological processes, including transepithelial fluid secretion, smooth muscle contraction , sensory signal transduction and others. CaCCs are considers as potential drug therapy of hypertension, secretoy diarrheas, neuropathic pain, asthma, cystic fibrosis and certain tumors. In our previous study, TMEM16A with green fluorescence p

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Liu, Dongli, Kai Wang, Danyan Su, et al. "TMEM16A Regulates Pulmonary Arterial Smooth Muscle Cells Proliferation via p38MAPK/ERK Pathway in High Pulmonary Blood Flow-Induced Pulmonary Arterial Hypertension." Journal of Vascular Research 58, no. 1 (2020): 27–37. http://dx.doi.org/10.1159/000511267.

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<b><i>Objective:</i></b> Pulmonary arterial hypertension (PAH) is a complex disease of the small pulmonary arteries that is mainly characterized by vascular remodeling. It has been demonstrated that excessive proliferation of pulmonary arterial smooth muscle cells (PASMCs) plays a pivotal role in vascular remodeling during PAH. The present study was undertaken to explore the role of TMEM16A in regulating PASMCs proliferation in high pulmonary blood flow-induced PAH. <b><i>Methods:</i></b> Aortocaval shunt surgery was undertaken to establish an an

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