Gene Symbol: Snta1
Description: syntrophin, acidic 1
Alias: AW228934, Snt1, alpha-1-syntrophin, 59 kDa dystrophin-associated protein A1 acidic component 1, alpha1-syntrophin, syntrophin-1
Species: mouse
Products:     Snta1

Top Publications

  1. Albrecht D, Sherman D, Brophy P, Froehner S. The ABCA1 cholesterol transporter associates with one of two distinct dystrophin-based scaffolds in Schwann cells. Glia. 2008;56:611-8 pubmed publisher
    ..Specifically, the cholesterol transporter ABCA1, associates with the Dp116/syntrophin complex in Cajal bands and is excluded from the DRP2/periaxin rich plaques...
  2. Hillier B, Christopherson K, Prehoda K, Bredt D, Lim W. Unexpected modes of PDZ domain scaffolding revealed by structure of nNOS-syntrophin complex. Science. 1999;284:812-5 pubmed
    ..This structure explains how PDZ domains can participate in diverse interaction modes to assemble protein networks. ..
  3. Bragg A, Amiry Moghaddam M, Ottersen O, Adams M, Froehner S. Assembly of a perivascular astrocyte protein scaffold at the mammalian blood-brain barrier is dependent on alpha-syntrophin. Glia. 2006;53:879-90 pubmed
  4. Kameya S, Miyagoe Y, Nonaka I, Ikemoto T, Endo M, Hanaoka K, et al. alpha1-syntrophin gene disruption results in the absence of neuronal-type nitric-oxide synthase at the sarcolemma but does not induce muscle degeneration. J Biol Chem. 1999;274:2193-200 pubmed
    ..Even though the distribution of nNOS was altered, the knock-out mice displayed no gross histological changes in the skeletal muscle. We also discovered that muscle contractile properties have not been influenced in the knock-out mice. ..
  5. Dmytrenko L, Cicanic M, Anderova M, Vorisek I, Ottersen O, Sykova E, et al. The impact of alpha-syntrophin deletion on the changes in tissue structure and extracellular diffusion associated with cell swelling under physiological and pathological conditions. PLoS ONE. 2013;8:e68044 pubmed publisher
    ..The substantially altered ECS diffusion parameters will likely affect the movement of neuroactive substances and/or trophic factors, which in turn may modulate the extent of tissue damage and/or drug distribution. ..
  6. Gavillet B, Rougier J, Domenighetti A, Behar R, Boixel C, Ruchat P, et al. Cardiac sodium channel Nav1.5 is regulated by a multiprotein complex composed of syntrophins and dystrophin. Circ Res. 2006;99:407-14 pubmed
    ..5. In the absence of dystrophin, decreased sodium current may explain the alterations in cardiac conduction observed in patients with dystrophinopathies. ..
  7. Neely J, Amiry Moghaddam M, Ottersen O, Froehner S, Agre P, Adams M. Syntrophin-dependent expression and localization of Aquaporin-4 water channel protein. Proc Natl Acad Sci U S A. 2001;98:14108-13 pubmed
    ..These results demonstrate that perivascular localization of AQP4 in brain requires alpha-Syn, and stability of AQP4 in the membrane is increased by the C-terminal PDZ-binding motif. ..
  8. Peters M, Adams M, Froehner S. Differential association of syntrophin pairs with the dystrophin complex. J Cell Biol. 1997;138:81-93 pubmed
    ..Since individual syntrophins do not have intrinsic binding specificity for dystrophin, dystrobrevin, or utrophin, the observed preferential pairing of syntrophins must depend on extrinsic regulatory mechanisms. ..
  9. Madhavan R, Jarrett H. Interactions between dystrophin glycoprotein complex proteins. Biochemistry. 1995;34:12204-9 pubmed
    ..The interactions identified here were used to refine the existing model of DGC organization to make it consistent with the current data. ..

More Information


  1. Adams M, Kramarcy N, Fukuda T, Engel A, Sealock R, Froehner S. Structural abnormalities at neuromuscular synapses lacking multiple syntrophin isoforms. J Neurosci. 2004;24:10302-9 pubmed
    ..We conclude that both alpha-syntrophin and beta2-syntrophin play distinct roles in forming and maintaining NMJ structure and that each syntrophin can partially compensate for the loss of the other. ..
  2. Brenman J, Chao D, Gee S, McGee A, Craven S, Santillano D, et al. Interaction of nitric oxide synthase with the postsynaptic density protein PSD-95 and alpha1-syntrophin mediated by PDZ domains. Cell. 1996;84:757-67 pubmed
    ..Interaction of PDZ-containing domains therefore mediates synaptic association of nNOS and may play a more general role in formation of macromolecular signaling complexes. ..
  3. Chen Z, Hague C, Hall R, Minneman K. Syntrophins regulate alpha1D-adrenergic receptors through a PDZ domain-mediated interaction. J Biol Chem. 2006;281:12414-20 pubmed
    ..This direct interaction may provide new information about the regulation of alpha1D-AR signaling and the role of syntrophins in modulating G protein-coupled receptor function. ..
  4. Luo S, Chen Y, Lai K, Arevalo J, Froehner S, Adams M, et al. {alpha}-Syntrophin regulates ARMS localization at the neuromuscular junction and enhances EphA4 signaling in an ARMS-dependent manner. J Cell Biol. 2005;169:813-24 pubmed
    ..Altogether, our findings suggest that ARMS may play an important role in regulating postsynaptic signal transduction through the syntrophin-mediated localization of receptor tyrosine kinases such as EphA4. ..
  5. Amiry Moghaddam M, Xue R, Haug F, Neely J, Bhardwaj A, Agre P, et al. Alpha-syntrophin deletion removes the perivascular but not endothelial pool of aquaporin-4 at the blood-brain barrier and delays the development of brain edema in an experimental model of acute hyponatremia. FASEB J. 2004;18:542-4 pubmed
    ..The resolution of the molecular basis and subcellular site of osmotically driven brain water uptake should help design new therapies for acute brain edema. ..
  6. Adams M, Kramarcy N, Krall S, Rossi S, Rotundo R, Sealock R, et al. Absence of alpha-syntrophin leads to structurally aberrant neuromuscular synapses deficient in utrophin. J Cell Biol. 2000;150:1385-98 pubmed
    ..Thus, alpha-syntrophin has an important role in synapse formation and in the organization of utrophin, acetylcholine receptor, and acetylcholinesterase at the neuromuscular synapse. ..
  7. Amiry Moghaddam M, Williamson A, Palomba M, Eid T, de Lanerolle N, Nagelhus E, et al. Delayed K+ clearance associated with aquaporin-4 mislocalization: phenotypic defects in brains of alpha-syntrophin-null mice. Proc Natl Acad Sci U S A. 2003;100:13615-20 pubmed
    ..These studies lead us to propose that water flux through perivascular AQP4 is needed to sustain efficient removal of K+ after neuronal activation. ..
  8. Percival J, Anderson K, Huang P, Adams M, Froehner S. Golgi and sarcolemmal neuronal NOS differentially regulate contraction-induced fatigue and vasoconstriction in exercising mouse skeletal muscle. J Clin Invest. 2010;120:816-26 pubmed publisher
    ..We conclude therefore that nNOS splice variants are critical regulators of skeletal muscle exercise performance. ..
  9. Piluso G, Mirabella M, Ricci E, Belsito A, Abbondanza C, Servidei S, et al. Gamma1- and gamma2-syntrophins, two novel dystrophin-binding proteins localized in neuronal cells. J Biol Chem. 2000;275:15851-60 pubmed
    ..Our present findings suggest a differentiated role of a modified dystrophin-associated complex in the central nervous system. ..
  10. Gorecki D, Abdulrazzak H, Lukasiuk K, Barnard E. Differential expression of syntrophins and analysis of alternatively spliced dystrophin transcripts in the mouse brain. Eur J Neurosci. 1997;9:965-76 pubmed
  11. Gee S, Madhavan R, Levinson S, Caldwell J, Sealock R, Froehner S. Interaction of muscle and brain sodium channels with multiple members of the syntrophin family of dystrophin-associated proteins. J Neurosci. 1998;18:128-37 pubmed
    ..Collectively, our data suggest that syntrophins link NaChs to the actin cytoskeleton and the extracellular matrix via dystrophin and the DAPC. ..
  12. Adams M, Mueller H, Froehner S. In vivo requirement of the alpha-syntrophin PDZ domain for the sarcolemmal localization of nNOS and aquaporin-4. J Cell Biol. 2001;155:113-22 pubmed
    ..Together, these data show that the sarcolemmal localization of nNOS and aquaporin-4 in vivo depends on the presence of a dystrophin-bound alpha-syntrophin PDZ domain. ..
  13. Hosaka Y, Yokota T, Miyagoe Suzuki Y, Yuasa K, Imamura M, Matsuda R, et al. Alpha1-syntrophin-deficient skeletal muscle exhibits hypertrophy and aberrant formation of neuromuscular junctions during regeneration. J Cell Biol. 2002;158:1097-107 pubmed
  14. Amiry Moghaddam M, Otsuka T, Hurn P, Traystman R, Haug F, Froehner S, et al. An alpha-syntrophin-dependent pool of AQP4 in astroglial end-feet confers bidirectional water flow between blood and brain. Proc Natl Acad Sci U S A. 2003;100:2106-11 pubmed
    ..The anchoring of AQP4 to alpha-syntrophin may be a target for treatment of brain edema, but therapeutic manipulations of AQP4 must consider the bidirectional water flux through this molecule. ..
  15. Ahn A, Freener C, Gussoni E, Yoshida M, Ozawa E, Kunkel L. The three human syntrophin genes are expressed in diverse tissues, have distinct chromosomal locations, and each bind to dystrophin and its relatives. J Biol Chem. 1996;271:2724-30 pubmed
  16. Ahn A, Yoshida M, Anderson M, Feener C, Selig S, Hagiwara Y, et al. Cloning of human basic A1, a distinct 59-kDa dystrophin-associated protein encoded on chromosome 8q23-24. Proc Natl Acad Sci U S A. 1994;91:4446-50 pubmed
    ..We have mapped the human basic component of A1 and EST25263 genes to chromosomes 8q23-24 and 16, respectively. ..
  17. Connors N, Adams M, Froehner S, Kofuji P. The potassium channel Kir4.1 associates with the dystrophin-glycoprotein complex via alpha-syntrophin in glia. J Biol Chem. 2004;279:28387-92 pubmed
    ..1 is localized in glial cells by its association with the DGC through a PDZ domain-mediated interaction with alpha-syntrophin and suggest an important role for the DGC in central nervous system physiology. ..
  18. Chockalingam P, Gee S, Jarrett H. Pleckstrin homology domain 1 of mouse alpha 1-syntrophin binds phosphatidylinositol 4,5-bisphosphate. Biochemistry. 1999;38:5596-602 pubmed
    ..Key residues in PtdIns4,5P2 binding to a PH domain were found to be conserved in alpha-syntrophins' PH1 domains and absent in PH2 domains, suggesting a molecular basis for binding. ..
  19. Adams M, Butler M, Dwyer T, Peters M, Murnane A, Froehner S. Two forms of mouse syntrophin, a 58 kd dystrophin-associated protein, differ in primary structure and tissue distribution. Neuron. 1993;11:531-40 pubmed
    ..Syntrophin-2 mRNAs (2.2, 5.0, and 10 kb) are expressed in all mouse tissues examined. These patterns of expression suggest that syntrophin-1 and syntrophin-2 may associate with different members of the dystrophin family. ..
  20. Adams M, Dwyer T, Dowler L, White R, Froehner S. Mouse alpha 1- and beta 2-syntrophin gene structure, chromosome localization, and homology with a discs large domain. J Biol Chem. 1995;270:25859-65 pubmed
    ..The first pleckstrin homology domain is interrupted by a domain homologous to repeated sequences originally found in the Drosophila discs-large protein. ..
  21. Sabourin J, Lamiche C, Vandebrouck A, Magaud C, Rivet J, Cognard C, et al. Regulation of TRPC1 and TRPC4 cation channels requires an alpha1-syntrophin-dependent complex in skeletal mouse myotubes. J Biol Chem. 2009;284:36248-61 pubmed publisher
    ..Cation channels with DAPC form a signaling complex that modulates cation entry and may be crucial for normal calcium homeostasis in skeletal muscles...
  22. Anderova M, Benesova J, Mikešová M, Dzamba D, Honsa P, Kriška J, et al. Altered astrocytic swelling in the cortex of α-syntrophin-negative GFAP/EGFP mice. PLoS ONE. 2014;9:e113444 pubmed publisher
    ..In summary, the deletion of α-syntrophin markedly alters astrocyte swelling during severe hypoosmotic stress, OGD or high K(+). ..
  23. Newbell B, Anderson J, Jarrett H. Ca2+-calmodulin binding to mouse alpha1 syntrophin: syntrophin is also a Ca2+-binding protein. Biochemistry. 1997;36:1295-305 pubmed
    ..Mouse alpha1 syntrophin binds the COOH-terminal domain of dystrophin, and calmodulin inhibits this interaction in a Ca2+-dependent ..
  24. Moon J, Choi S, Heo C, Kim H, Kim H. α-Syntrophin stabilizes catalase to reduce endogenous reactive oxygen species levels during myoblast differentiation. FEBS J. 2017;284:2052-2065 pubmed publisher
    ..This protein plays an important role in the regulation of oxidative stress from endogenously generated ROS during myoblast differentiation by modulating the protein stability of catalase. ..
  25. Oak S, Russo K, Petrucci T, Jarrett H. Mouse alpha1-syntrophin binding to Grb2: further evidence of a role for syntrophin in cell signaling. Biochemistry. 2001;40:11270-8 pubmed
    ..Grb2-C-SH3 domain bound syntrophin with slightly higher affinity than Grb2-N-SH3 domain. Crk-L, an SH2/SH3 protein of similar domain structure but different specificity, does not bind these syntrophin sequences. ..
  26. Zhou Y, Oak S, Senogles S, Jarrett H. Laminin-alpha1 globular domains 3 and 4 induce heterotrimeric G protein binding to alpha-syntrophin's PDZ domain and alter intracellular Ca2+ in muscle. Am J Physiol Cell Physiol. 2005;288:C377-88 pubmed
    ..These observations suggest that DGC is a matrix laminin, G protein-coupled receptor. ..
  27. Kim M, Froehner S, Adams M, Kim H. ?-Syntrophin is required for the hepatocyte growth factor-induced migration of cultured myoblasts. Exp Cell Res. 2011;317:2914-24 pubmed publisher
    ..Phosphorylation of Akt was reduced in the ?-syntrophin siRNA-treated C2 cells. These results suggest that ?-syntrophin is required for HGF-induced migration of myoblasts and for proper PI3-kinase/Akt signaling. ..
  28. Lim J, Choi S, Moon J, Kim H. ?-Syntrophin is involved in the survival signaling pathway in myoblasts under menadione-induced oxidative stress. Exp Cell Res. 2016;344:1-10 pubmed publisher
    ..These results suggest that ?-syntrophin plays a pivotal role in the survival pathway triggered by menadione-induced oxidative stress in cultured myoblasts. ..
  29. Ang S, Uebersohn A, Spencer C, Huang Y, Lee J, Ge K, et al. KMT2D regulates specific programs in heart development via histone H3 lysine 4 di-methylation. Development. 2016;143:810-21 pubmed publisher
    ..Our findings indicate that KMT2D is essential for regulating cardiac gene expression during heart development primarily via H3K4 di-methylation. ..
  30. Enger R, Gundersen G, Haj Yasein N, Eilert Olsen M, Thorén A, Vindedal G, et al. Molecular scaffolds underpinning macroglial polarization: an analysis of retinal Müller cells and brain astrocytes in mouse. Glia. 2012;60:2018-26 pubmed publisher
    ..These data indicate that the molecular scaffolding in perivascular endfeet is more complex than previously assumed and that macroglia are heterogeneous with respect to the mechanisms that dictate their polarization. ..
  31. Thomas G, Shaul P, Yuhanna I, Froehner S, Adams M. Vasomodulation by skeletal muscle-derived nitric oxide requires alpha-syntrophin-mediated sarcolemmal localization of neuronal Nitric oxide synthase. Circ Res. 2003;92:554-60 pubmed
  32. Williams J, Armesilla A, Mohamed T, Hagarty C, McIntyre F, Schomburg S, et al. The sarcolemmal calcium pump, alpha-1 syntrophin, and neuronal nitric-oxide synthase are parts of a macromolecular protein complex. J Biol Chem. 2006;281:23341-8 pubmed
    ..In conclusion, the present data demonstrate for the first time the localization of PMCA1b and -4b to the syntrophin.dystrophin complex in the heart and provide a specific molecular mechanism of interaction as well as functionality. ..
  33. Eilert Olsen M, Haj Yasein N, Vindedal G, Enger R, Gundersen G, Hoddevik E, et al. Deletion of aquaporin-4 changes the perivascular glial protein scaffold without disrupting the brain endothelial barrier. Glia. 2012;60:432-40 pubmed publisher
    ..Our data also indicate that AQP4 and ?-syntrophin are mutually dependent upon each other for proper perivascular expression. ..
  34. Ueda K, Valdivia C, Medeiros Domingo A, Tester D, Vatta M, Farrugia G, et al. Syntrophin mutation associated with long QT syndrome through activation of the nNOS-SCN5A macromolecular complex. Proc Natl Acad Sci U S A. 2008;105:9355-60 pubmed publisher
    ..Direct sequencing of SNTA1, the gene encoding alpha1-syntrophin, was performed in a cohort of LQTS patients that were negative for mutations ..
  35. Blake D, Hawkes R, Benson M, Beesley P. Different dystrophin-like complexes are expressed in neurons and glia. J Cell Biol. 1999;147:645-58 pubmed
    ..Thus, despite the similarity in primary sequence, alpha- and beta-dystrobrevin are differentially distributed in the brain where they form separate DPC-like complexes. ..
  36. Matsumura K, Ervasti J, Ohlendieck K, Kahl S, Campbell K. Association of dystrophin-related protein with dystrophin-associated proteins in mdx mouse muscle. Nature. 1992;360:588-91 pubmed
    ..Because these muscles show minimal pathological changes, our results could provide a basis for the upregulation of DRP as a potential therapeutic approach. ..
  37. Harris B, Lau F, Fujii N, Guy R, Lim W. Role of electrostatic interactions in PDZ domain ligand recognition. Biochemistry. 2003;42:2797-805 pubmed
    ..Peptides with a free carboxy terminus, or presented within a specific structural context, can satisfy these requirements. ..
  38. Joe M, Kee C, Tomarev S. Myocilin interacts with syntrophins and is member of dystrophin-associated protein complex. J Biol Chem. 2012;287:13216-27 pubmed publisher
    ..We suggest that intracellular myocilin plays a role as a regulator of muscle hypertrophy pathways, acting through the components of DAPC. ..
  39. Kim M, Hwang S, Lim J, Froehner S, Adams M, Kim H. ?-syntrophin modulates myogenin expression in differentiating myoblasts. PLoS ONE. 2010;5:e15355 pubmed publisher
    ..We conclude that ?-syntrophin plays an important role in regulating myogenesis by modulating myogenin expression. ..
  40. Hebel T, Eisinger K, Neumeier M, Rein Fischboeck L, Pohl R, Meier E, et al. Lipid abnormalities in alpha/beta2-syntrophin null mice are independent from ABCA1. Biochim Biophys Acta. 2015;1851:527-36 pubmed publisher
    ..Current data exclude a major function of these syntrophins in ABCA1 activity and insulin release but suggest a role in regulating glucose uptake, ERK and SR-BI levels, and sphingomyelin metabolism in obesity. ..
  41. Hagiwara Y, Sasaoka T, Araishi K, Imamura M, Yorifuji H, Nonaka I, et al. Caveolin-3 deficiency causes muscle degeneration in mice. Hum Mol Genet. 2000;9:3047-54 pubmed
    ..No apparent muscle degeneration was observed in heterozygous mutant mice, indicating that pathological changes caused by caveolin-3 gene disruption were inherited through the recessive form of genetic transmission. ..
  42. Madhavan R, Jarrett H. Phosphorylation of dystrophin and alpha-syntrophin by Ca(2+)-calmodulin dependent protein kinase II. Biochim Biophys Acta. 1999;1434:260-74 pubmed
    ..We also show that phosphorylation of the dystrophin C terminal domain sequences inhibits their syntrophin binding in vitro, suggesting a regulatory role for phosphorylation. ..
  43. Adams M, Anderson K, Froehner S. The alpha-syntrophin PH and PDZ domains scaffold acetylcholine receptors, utrophin, and neuronal nitric oxide synthase at the neuromuscular junction. J Neurosci. 2010;30:11004-10 pubmed publisher
    ..We conclude that the PH1 and PDZ domains of alpha-syntrophin work in concert to facilitate the localization of AChRs and nNOS at the NMJ. ..
  44. Benabdesselam R, Dorbani Mamine L, Benmessaoud Mesbah O, Rendon A, Mhaouty Kodja S, Hardin Pouzet H. Dp71 gene disruption alters the composition of the dystrophin-associated protein complex and neuronal nitric oxide synthase expression in the hypothalamic supraoptic and paraventricular nuclei. J Endocrinol. 2012;213:239-49 pubmed publisher
    ..Such DAPC disorganization may lead to modification of the microenvironment of the SON and PVN neurons and thus may result in a perturbed osmoregulation. ..
  45. Eisinger K, Rein Fischboeck L, Pohl R, Meier E, Krautbauer S, Buechler C. The adaptor protein alpha-syntrophin regulates adipocyte lipid droplet growth. Exp Cell Res. 2016;345:100-7 pubmed publisher
    ..Enhanced preadipocyte proliferation and capacity to store surplus fatty acids may protect adipocytes with low SNTA from lipotoxicity in obesity. ..
  46. Martinez Pena y Valenzuela I, Mouslim C, Pires Oliveira M, Adams M, Froehner S, Akaaboune M. Nicotinic acetylcholine receptor stability at the NMJ deficient in ?-syntrophin in vivo. J Neurosci. 2011;31:15586-96 pubmed publisher
    ..These results demonstrate that ?-syn is required for the maturation and stability of the postsynaptic apparatus and suggest that ?-syn may act via ?-dbn1. ..
  47. Aquilano K, Baldelli S, Ciriolo M. Nuclear recruitment of neuronal nitric-oxide synthase by ?-syntrophin is crucial for the induction of mitochondrial biogenesis. J Biol Chem. 2014;289:365-78 pubmed publisher
    ..Overall, our results indicate that altered nNOS splicing and nuclear localization could be contributing factors in human muscular diseases associated with mitochondrial impairment. ..
  48. Cruz N, Ball K, Froehner S, Adams M, Dienel G. Regional registration of [6-(14)C]glucose metabolism during brain activation of ?-syntrophin knockout mice. J Neurochem. 2013;125:247-59 pubmed publisher
    ..The results suggest a role for AQP4-mediated water flow in support of washout of metabolites, and underscore the need for greater understanding of astrocytic water and metabolite fluxes. ..
  49. Fuhrmann Stroissnigg H, Noiges R, Descovich L, Fischer I, Albrecht D, Nothias F, et al. The light chains of microtubule-associated proteins MAP1A and MAP1B interact with ?1-syntrophin in the central and peripheral nervous system. PLoS ONE. 2012;7:e49722 pubmed publisher
  50. Shou W, Aghdasi B, Armstrong D, Guo Q, Bao S, Charng M, et al. Cardiac defects and altered ryanodine receptor function in mice lacking FKBP12. Nature. 1998;391:489-92 pubmed
    ..Physiological studies demonstrate that FKBP12 is dispensable for TGF-beta-mediated signalling, but modulates the calcium release activity of both skeletal and cardiac ryanodine receptors. ..
  51. Suzuki N, Motohashi N, Uezumi A, Fukada S, Yoshimura T, Itoyama Y, et al. NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS. J Clin Invest. 2007;117:2468-76 pubmed
    ..We conclude that nNOS/NO mediates muscle atrophy via regulation of Foxo transcription factors and is a new therapeutic target for disuse-induced muscle atrophy. ..
  52. McAndrew P, Frostholm A, White R, Rotter A, Burghes A. Identification and characterization of RPTP rho, a novel RPTP mu/kappa-like receptor protein tyrosine phosphatase whose expression is restricted to the central nervous system. Brain Res Mol Brain Res. 1998;56:9-21 pubmed
  53. Oak S, Jarrett H. Oligomerization of mouse alpha 1-syntrophin and self-association of its pleckstrin homology domain 1 containing sequences. Biochemistry. 2000;39:8870-7 pubmed
    ..Since calmodulin inhibited syntrophin oligomerization in the presence or absence of Ca(2+), Ca(2+) binding to syntrophin is responsible for the inhibition by EGTA of syntrophin oligomerization. ..
  54. Munehira Y, Ohnishi T, Kawamoto S, Furuya A, Shitara K, Imamura M, et al. Alpha1-syntrophin modulates turnover of ABCA1. J Biol Chem. 2004;279:15091-5 pubmed
    ..These results suggest that alpha1-syntrophin is involved in intracellular signaling, which determines the stability of ABCA1 and modulates cellular cholesterol release...
  55. Shiao T, Fond A, Deng B, Wehling Henricks M, Adams M, Froehner S, et al. Defects in neuromuscular junction structure in dystrophic muscle are corrected by expression of a NOS transgene in dystrophin-deficient muscles, but not in muscles lacking alpha- and beta1-syntrophins. Hum Mol Genet. 2004;13:1873-84 pubmed
    ..The results suggest that defects in NMJ structure that occur in some DGC mutants can result from the secondary loss of NOS from muscle. ..
  56. Yan J, Wen W, Xu W, Long J, Adams M, Froehner S, et al. Structure of the split PH domain and distinct lipid-binding properties of the PH-PDZ supramodule of alpha-syntrophin. EMBO J. 2005;24:3985-95 pubmed
    ..We further showed that the PH(N)-PDZ-PH(C) tandem forms a functionally distinct supramodule, in which the split PH domain and the PDZ domain function synergistically in binding to inositol phospholipids. ..
  57. Yakubchyk Y, Abramovici H, Maillet J, Daher E, Obagi C, Parks R, et al. Regulation of neurite outgrowth in N1E-115 cells through PDZ-mediated recruitment of diacylglycerol kinase zeta. Mol Cell Biol. 2005;25:7289-302 pubmed
    ..Collectively, these findings suggest DGK-zeta, syntrophin, and Rac1 form a regulated signaling complex that controls polarized outgrowth in neuronal cells. ..
  58. Hibino H, Fujita A, Iwai K, Yamada M, Kurachi Y. Differential assembly of inwardly rectifying K+ channel subunits, Kir4.1 and Kir5.1, in brain astrocytes. J Biol Chem. 2004;279:44065-73 pubmed
    ..D'Adamo, M. C., and Pessia, M. (2000) J. Biol. Chem. 275, 16404-16407), it is plausible that these channels play differential physiological roles in the K+ -buffering action of brain astrocytes in a region-specific manner. ..
  59. Puwarawuttipanit W, Bragg A, Frydenlund D, Mylonakou M, Nagelhus E, Peters M, et al. Differential effect of alpha-syntrophin knockout on aquaporin-4 and Kir4.1 expression in retinal macroglial cells in mice. Neuroscience. 2006;137:165-75 pubmed
    ..1 and the alpha-syntrophin independent pool of aquaporin-4. ..
  60. Johnson E, Zhang L, Adams M, Phillips A, Freitas M, Froehner S, et al. Proteomic analysis reveals new cardiac-specific dystrophin-associated proteins. PLoS ONE. 2012;7:e43515 pubmed publisher
    ..In addition, our findings support the existence of cardiac-specific functions of dystrophin and may guide studies into early triggers of cardiac disease in Duchenne and Becker muscular dystrophies. ..