Coxsackievirus and adenovirus receptor

Last updated
CXADR
Protein CXADR PDB 1eaj.png
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases CXADR , CAR, CAR4/6, HCAR, coxsackie virus and adenovirus receptor, Ig-like cell adhesion molecule, CXADR Ig-like cell adhesion molecule
External IDs OMIM: 602621 MGI: 1201679 HomoloGene: 1024 GeneCards: CXADR
Orthologs
SpeciesHumanMouse
Entrez

1525

13052

Ensembl

ENSG00000154639

ENSMUSG00000022865

UniProt

P78310

P97792

RefSeq (mRNA)

NM_001207063
NM_001207064
NM_001207065
NM_001207066
NM_001338

NM_001025192
NM_001276263
NM_009988

RefSeq (protein)

NP_001193992
NP_001193993
NP_001193994
NP_001193995
NP_001329

NP_001020363
NP_001263192
NP_034118

Location (UCSC) Chr 21: 17.51 – 17.59 Mb Chr 16: 78.1 – 78.16 Mb
PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Coxsackievirus and adenovirus receptor (CAR) is a protein that in humans is encoded by the CXADR gene. [5] [6] [7] The protein encoded by this gene is a type I membrane receptor for group B coxsackie viruses and subgroup C adenoviruses. CAR protein is expressed in several tissues, including heart, brain, and, more generally, epithelial and endothelial cells. In cardiac muscle, CAR is localized to intercalated disc structures, which electrically and mechanically couple adjacent cardiomyocytes. CAR plays an important role in the pathogenesis of myocarditis, dilated cardiomyopathy, and in arrhythmia susceptibility following myocardial infarction or myocardial ischemia. In addition, an isoform of CAR (CAR-SIV) has been recently identified in the cytoplasm of pancreatic beta cells. It's been suggested that CAR-SIV resides in the insulin secreting granules and might be involved in the virus infection of these cells. [8]

Structure

Human CAR protein has a theoretical molecular weight of 40.0 kDa and is composed of 365 amino acids. [9] The human CAR gene (CXADR) is found on chromosome 21. Alternative splicing is known to produce at least 2 splice variants known as hCAR1 and hCAR2 and are each composed of at least 7 exons. Pseudogenes of this gene are found on chromosomes 15, 18, and 21. [7]

CAR is a transmembrane bound protein with two Ig-like extracellular domains, a transmembrane domain, a cytoplasmic domain, and two N-linked glycosylation sites. CAR contains two disulfide bonded loops (residues 35-130 and 155-220). [10] The N-terminal segment comprises the two extracellular domains (D1 and D2). D1 is most distal from the membrane and contains a V/Ig-like fold whereas D2 is more proximal. The cytoplasmic tail of CAR contains the amino acids G S I V, which is characterized as a class 1 PDZ-binding motif for interacting with proteins containing PDZ domains. [11]

The protein is found to be expressed in various regions of the body including the heart, brain, and, more generally, epithelial and endothelial cells. Moreover, CAR expression is not found in normal or tumor cell lines. Expression of CAR in endothelial cells can be regulated by treatment with drugs. [12] [13]

Function

It functions as a homophilic and heterophilic cell adhesion molecule through its interactions with extracellular matrix glycoproteins such as: fibronectin, agrin, laminin-1 and tenascin-R. [14] In addition, it is thought to regulate the cytoskeleton through interactions with actin and microtubules. Moreover, its cytoplasmic domain contains putative phosphorylation sites and a PDZ-interaction motif which suggests a scaffolding role.[ citation needed ]

Cardiac

CAR is essential for normal development of cardiomyocytes. The expression of CAR is high in developing tissues, including the heart and brain; postnatally it is expressed in epithelial cells and in adult cardiac muscle, it is localized at intercalated discs. [15] Knocking out CAR is embryonic lethal in mice by day 11.5, coordinate with severe cardiac muscle abnormalities including left ventricular hyperplasia, sinuatrial valve abnormalities, pericardial edema, thoracic hemorrhaging, myocardial wall degeneration, regional apoptosis, reduced density and disorganization of myofibrils, and enlarged mitochondria. [16] [17] [18] Cardiomyocyte-specific deletion of CAR after embryonic day 11 had no noticeable effect on development and postnatal life, suggesting that CAR is critical during a temporal window of cardiac development. [18]

It is clear from studies employing transgenesis that CAR function at intercalated discs in cardiac muscle is critical for normal heart function. Cardiac-specific knockout of CAR causes first degree block or complete block in the propagation of electrical conduction in the AV node. This was coordinate with the loss of connexin-45 at cell-cell junctions on the sarcolemmal membranes of AV node cells. Mice eventually developed cardiomyopathy associated with intercalated disc disorganization and loss of cardiomyocyte beta-catenin and ZO-1 expression; studies also showed that CAR, and connexin-45 form a protein complex that requires the PDZ-binding motif on CAR for proper formation. Moreover, CAR is required for normal localization of connexin-45, beta-catenin and ZO-1 at intercalated discs. [19]

Studies from human hearts have shown that lower expression of CXADR mRNA is associated with a risk allele at chromosome 21q21, which may in fact predispose hearts to arrhythmias. To discern the mechanistic underpinnings, hearts from heterozygous CAR knockout mice subjected to acute myocardial ischemia were evaluated and showed slowed ventricular conduction, earlier onset of ventricular arrhythmias, and increased susceptibility to arrhythmias. These findings were coordinate with a reduction in magnitude of the sodium current at intercalated discs; CAR coprecipitated with NaV1.5, which may provide a mechanistic link to this finding. [20]

Neural and lymphatic

CAR is strongly expressed in the developing central nervous system where it is thought to mediate neurite outgrowth. In addition, expression of CAR is readily detectable in the adult nervous system. [14]

It has also been shown that CAR is critical for the development of lymphatic vasculature and in forming lymphatic endothelial cell-cell junctions. [21]

Clinical significance

CAR is a receptor for both Coxsackie B virus and adenovirus 2 and 5, which are structurally distinct. [22]

In patients with myocarditis or dilated cardiomyopathy, elevated Coxsackie B2 viral nucleic acids have been detected in myocardial biopsy samples. [23] Adenoviral genomic DNA has also been detected in myocardial biopsies of patients with idiopathic cardiomyopathy, or impaired left ventricular function of unknown origin. [24] Patients exhibiting sudden death from acute myocardial infarction had a higher proportion of active coxsackie B virus infection relative to matched controls, which was coordinate with disrupted sarcolemmal localization of dystrophin, suggesting that enteroviral infection may worsen the outcome of patients with acute myocardial infarction. [25]

A role for CAR in arrhythmia susceptibility and ventricular fibrillation after myocardial infarction was shown in that CXADR lies near the 21q21 locus, which is strongly associated with these insults. [20] [26] [27] [28]

Interactions

CAR has been shown to interact with: MAGI-1b, [11] PICK1, [11] PSD-95, [11] ZO-1, [29] NaV1.5 [20]

Related Research Articles

Coxsackie B4 virus are enteroviruses that belong to the Picornaviridae family. These viruses can be found worldwide. They are positive-sense, single-stranded, non-enveloped RNA viruses with icosahedral geometry. Coxsackieviruses have two groups, A and B, each associated with different diseases. Coxsackievirus group A is known for causing hand-foot-and-mouth diseases while Group B, which contains six serotypes, can cause a varying range of symptoms like gastrointestinal distress myocarditis. Coxsackievirus B4 has a cell tropism for natural killer cells and pancreatic islet cells. Infection can lead to beta cell apoptosis which increases the risk of insulitis.

<span class="mw-page-title-main">Coxsackievirus</span> Virus that causes digestive upset and sometimes heart damage

Coxsackieviruses are a few related enteroviruses that belong to the Picornaviridae family of nonenveloped, linear, positive-sense single-stranded RNA viruses, as well as its genus Enterovirus, which also includes poliovirus and echovirus. Enteroviruses are among the most common and important human pathogens, and ordinarily its members are transmitted by the fecal–oral route. Coxsackieviruses share many characteristics with poliovirus. With control of poliovirus infections in much of the world, more attention has been focused on understanding the nonpolio enteroviruses such as coxsackievirus.

<span class="mw-page-title-main">Coxsackie B virus</span> Virus that causes digestive upset and sometimes heart damage

Coxsackie B is a group of six serotypes of coxsackievirus (CVB1-CVB6), a pathogenic enterovirus, that trigger illness ranging from gastrointestinal distress to full-fledged pericarditis and myocarditis.

<span class="mw-page-title-main">Cardiac muscle</span> Muscular tissue of heart in vertebrates

Cardiac muscle is one of three types of vertebrate muscle tissues, with the other two being skeletal muscle and smooth muscle. It is an involuntary, striated muscle that constitutes the main tissue of the wall of the heart. The cardiac muscle (myocardium) forms a thick middle layer between the outer layer of the heart wall and the inner layer, with blood supplied via the coronary circulation. It is composed of individual cardiac muscle cells joined by intercalated discs, and encased by collagen fibers and other substances that form the extracellular matrix.

<span class="mw-page-title-main">Myocarditis</span> Inflammation of the heart muscle

Myocarditis, also known as inflammatory cardiomyopathy, is an acquired cardiomyopathy due to inflammation of the heart muscle. Symptoms can include shortness of breath, chest pain, decreased ability to exercise, and an irregular heartbeat. The duration of problems can vary from hours to months. Complications may include heart failure due to dilated cardiomyopathy or cardiac arrest.

<i>Adenoviridae</i> Family of viruses

Adenoviruses are medium-sized, nonenveloped viruses with an icosahedral nucleocapsid containing a double-stranded DNA genome. Their name derives from their initial isolation from human adenoids in 1953.

<span class="mw-page-title-main">Dilated cardiomyopathy</span> Medical condition

Dilated cardiomyopathy (DCM) is a condition in which the heart becomes enlarged and cannot pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Complications can include heart failure, heart valve disease, or an irregular heartbeat.

<span class="mw-page-title-main">Desmoglein-2</span> Protein found in humans

Desmoglein-2 is a protein that in humans is encoded by the DSG2 gene. Desmoglein-2 is highly expressed in epithelial cells and cardiomyocytes. Desmoglein-2 is localized to desmosome structures at regions of cell-cell contact and functions to structurally adhere adjacent cells together. In cardiac muscle, these regions are specialized regions known as intercalated discs. Mutations in desmoglein-2 have been associated with arrhythmogenic right ventricular cardiomyopathy and familial dilated cardiomyopathy.

<span class="mw-page-title-main">Plakoglobin</span> Mammalian protein found in Homo sapiens

Plakoglobin, also known as junction plakoglobin or gamma-catenin, is a protein that in humans is encoded by the JUP gene. Plakoglobin is a member of the catenin protein family and homologous to β-catenin. Plakoglobin is a cytoplasmic component of desmosomes and adherens junctions structures located within intercalated discs of cardiac muscle that function to anchor sarcomeres and join adjacent cells in cardiac muscle. Mutations in plakoglobin are associated with arrhythmogenic right ventricular dysplasia.

<span class="mw-page-title-main">Cadherin-2</span> Protein-coding gene in the species Homo sapiens

Cadherin-2 also known as Neural cadherin (N-cadherin), is a protein that in humans is encoded by the CDH2 gene. CDH2 has also been designated as CD325 . Cadherin-2 is a transmembrane protein expressed in multiple tissues and functions to mediate cell–cell adhesion. In cardiac muscle, Cadherin-2 is an integral component in adherens junctions residing at intercalated discs, which function to mechanically and electrically couple adjacent cardiomyocytes. Alterations in expression and integrity of Cadherin-2 has been observed in various forms of disease, including human dilated cardiomyopathy. Variants in CDH2 have also been identified to cause a syndromic neurodevelopmental disorder.

<span class="mw-page-title-main">Ryanodine receptor 2</span> Transport protein and coding gene in humans

Ryanodine receptor 2 (RYR2) is one of a class of ryanodine receptors and a protein found primarily in cardiac muscle. In humans, it is encoded by the RYR2 gene. In the process of cardiac calcium-induced calcium release, RYR2 is the major mediator for sarcoplasmic release of stored calcium ions.

<span class="mw-page-title-main">DSC2</span> Protein-coding gene in humans

Desmocollin-2 is a protein that in humans is encoded by the DSC2 gene. Desmocollin-2 is a cadherin-type protein that functions to link adjacent cells together in specialized regions known as desmosomes. Desmocollin-2 is widely expressed, and is the only desmocollin isoform expressed in cardiac muscle, where it localizes to intercalated discs. Mutations in DSC2 have been causally linked to arrhythmogenic right ventricular cardiomyopathy.

<span class="mw-page-title-main">Plakophilin-2</span> Protein-coding gene in the species Homo sapiens

Plakophilin-2 is a protein that in humans is encoded by the PKP2 gene. Plakophilin 2 is expressed in skin and cardiac muscle, where it functions to link cadherins to intermediate filaments in the cytoskeleton. In cardiac muscle, plakophilin-2 is found in desmosome structures located within intercalated discs. Mutations in PKP2 have been shown to be causal in arrhythmogenic right ventricular cardiomyopathy.

JAML or Junctional Adhesion Molecule-Like, or AMICA1 is a JAM transmembrane protein family member. It is composed of two extracellular immunoglobulin-like domains, a membrane-spanning region, and a cytoplasmic tail involved in activation signaling. A known ligand of JAML is Coxsackie virus and Adenovirus Receptor which has been shown to localize to the tight junctions of epithelial cells.

<span class="mw-page-title-main">Ankyrin-2</span> Protein-coding gene in the species Homo sapiens

Ankyrin-2, also known as Ankyrin-B, and Brain ankyrin, is a protein which in humans is encoded by the ANK2 gene. Ankyrin-2 is ubiquitously expressed, but shows high expression in cardiac muscle. Ankyrin-2 plays an essential role in the localization and membrane stabilization of ion transporters and ion channels in cardiomyocytes, as well as in costamere structures. Mutations in ANK2 cause a dominantly-inherited, cardiac arrhythmia syndrome known as long QT syndrome 4 as well as sick sinus syndrome; mutations have also been associated to a lesser degree with hypertrophic cardiomyopathy. Alterations in ankyrin-2 expression levels are observed in human heart failure.

Beta adrenergic receptor kinase carboxyl-terminus is a peptide composed of the last 194 amino acid residues of the carboxyl-terminus of beta adrenergic receptor kinase 1 (βARK1). It binds the βγ subunits of G proteins located in the plasma membrane of cells. It is currently an experimental gene therapy for the treatment of heart failure.

Human HGF plasmid DNA therapy of cardiomyocytes is being examined as a potential treatment for coronary artery disease, as well as treatment for the damage that occurs to the heart after MI. After MI, the myocardium suffers from reperfusion injury which leads to death of cardiomyocytes and detrimental remodelling of the heart, consequently reducing proper cardiac function. Transfection of cardiac myocytes with human HGF reduces ischemic reperfusion injury after MI. The benefits of HGF therapy include preventing improper remodelling of the heart and ameliorating heart dysfunction post-MI.

sCAR-Fc is an experimental prophylactic treatment against coxsackievirus B3 (CVB) infections. Coxsackievirus B3 can cause cardiac damage, eventually resulting in a weakened and enlarged heart that is termed dilated cardiomyopathy. While many other treatments inhibit viral proliferation in myocytes, sCAR-Fc prevents the virus entering the cell by competitively binding to coxsackie virus and adenovirus receptors (CAR) on the membrane of myocytes.

Coxsackieviruses-induced cardiomyopathy are positive-stranded RNA viruses in picornavirus family and the genus enterovirus, acute enterovirus infections such as Coxsackievirus B3 have been identified as the cause of virally induced acute myocarditis, resulting in dilated cardiomyopathy. Dilated cardiomyopathy in humans can be caused by multiple factors including hereditary defects in the cytoskeletal protein dystrophin in Duchenne muscular dystrophy (DMD) patients). A heart that undergoes dilated cardiomyopathy shows unique enlargement of ventricles, and thinning of the ventricular wall that may lead to heart failure. In addition to the genetic defects in dystrophin or other cytoskeletal proteins, a subset of dilated cardiomyopathy is linked to enteroviral infection in the heart, especially coxsackievirus B. Enterovirus infections are responsible for about 30% of the cases of acquired dilated cardiomyopathy in humans.

Heart problems are more common in people with HIV/AIDS. Those with left ventricular dysfunction have a median survival of 101 days as compared to 472 days in people with AIDS with healthy hearts. HIV is a major cause of cardiomyopathy. The most common type of HIV induced cardiomyopathy is dilated cardiomyopathy also known as eccentric ventricular hypertrophy which leads to impaired contraction of the ventricles due to volume overload. The annual incidence of HIV associated dilated cardiomyopathy was 15.9/1000 before the introduction of highly active antiretroviral therapy (HAART). However, in 2014, a study found that 17.6% of HIV patients have dilated cardiomyopathy (176/1000) meaning the incidence has greatly increased.

References

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000154639 - Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000022865 - Ensembl, May 2017
  3. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ↑ Bergelson JM, Cunningham JA, Droguett G, Kurt-Jones EA, Krithivas A, Hong JS, Horwitz MS, Crowell RL, Finberg RW (Feb 1997). "Isolation of a common receptor for Coxsackie B viruses and adenoviruses 2 and 5". Science. 275 (5304): 1320–3. doi:10.1126/science.275.5304.1320. PMID   9036860. S2CID   33824689.
  6. ↑ Tomko RP, Xu R, Philipson L (Apr 1997). "HCAR and MCAR: the human and mouse cellular receptors for subgroup C adenoviruses and group B coxsackieviruses". Proceedings of the National Academy of Sciences of the United States of America. 94 (7): 3352–6. Bibcode:1997PNAS...94.3352T. doi: 10.1073/pnas.94.7.3352 . PMC   20373 . PMID   9096397.
  7. 1 2 "Entrez Gene: CXADR coxsackie virus and adenovirus receptor".
  8. ↑ Ifie, Eseoghene; Russell, Mark A.; Dhayal, Shalinee; Leete, Pia; Sebastiani, Guido; Nigi, Laura; Dotta, Francesco; Marjomäki, Varpu; Eizirik, Decio L.; Morgan, Noel G.; Richardson, Sarah J. (November 2018). "Unexpected subcellular distribution of a specific isoform of the Coxsackie and adenovirus receptor, CAR-SIV, in human pancreatic beta cells". Diabetologia. 61 (11): 2344–2355. doi:10.1007/s00125-018-4704-1. ISSN   1432-0428. PMC   6182664 . PMID   30074059.
  9. ↑ "Protein sequence of human CXADR (Uniprot ID: P78310)". Cardiac Organellar Protein Atlas Knowledgebase (COPaKB). Archived from the original on 15 July 2015. Retrieved 14 July 2015.
  10. ↑ Tomko RP, Xu R, Philipson L (Apr 1997). "HCAR and MCAR: the human and mouse cellular receptors for subgroup C adenoviruses and group B coxsackieviruses". Proceedings of the National Academy of Sciences of the United States of America. 94 (7): 3352–6. Bibcode:1997PNAS...94.3352T. doi: 10.1073/pnas.94.7.3352 . PMC   20373 . PMID   9096397.
  11. 1 2 3 4 Excoffon KJ, Hruska-Hageman A, Klotz M, Traver GL, Zabner J (Sep 2004). "A role for the PDZ-binding domain of the coxsackie B virus and adenovirus receptor (CAR) in cell adhesion and growth". Journal of Cell Science. 117 (Pt 19): 4401–9. doi: 10.1242/jcs.01300 . PMID   15304526.
  12. ↑ Funke C, Farr M, Werner B, Dittmann S, Uberla K, Piper C, Niehaus K, Horstkotte D (Aug 2010). "Antiviral effect of Bosentan and Valsartan during coxsackievirus B3 infection of human endothelial cells". The Journal of General Virology. 91 (Pt 8): 1959–70. doi: 10.1099/vir.0.020065-0 . PMID   20392896.
  13. ↑ Werner B, Dittmann S, Funke C, Überla K, Piper C, Niehaus K, Horstkotte D, Farr M (Apr 2014). "Effect of lovastatin on coxsackievirus B3 infection in human endothelial cells". Inflammation Research. 63 (4): 267–76. doi:10.1007/s00011-013-0695-z. PMID   24316867. S2CID   18722233.
  14. 1 2 Patzke C, Max KE, Behlke J, Schreiber J, Schmidt H, Dorner AA, Kröger S, Henning M, Otto A, Heinemann U, Rathjen FG (Feb 2010). "The coxsackievirus-adenovirus receptor reveals complex homophilic and heterophilic interactions on neural cells". The Journal of Neuroscience. 30 (8): 2897–910. doi:10.1523/JNEUROSCI.5725-09.2010. PMC   6633923 . PMID   20181587.
  15. ↑ Kashimura T, Kodama M, Hotta Y, Hosoya J, Yoshida K, Ozawa T, Watanabe R, Okura Y, Kato K, Hanawa H, Kuwano R, Aizawa Y (Mar 2004). "Spatiotemporal changes of coxsackievirus and adenovirus receptor in rat hearts during postnatal development and in cultured cardiomyocytes of neonatal rat". Virchows Archiv. 444 (3): 283–92. doi:10.1007/s00428-003-0925-9. PMID   14624362. S2CID   768724.
  16. ↑ Asher DR, Cerny AM, Weiler SR, Horner JW, Keeler ML, Neptune MA, Jones SN, Bronson RT, Depinho RA, Finberg RW (Jun 2005). "Coxsackievirus and adenovirus receptor is essential for cardiomyocyte development". Genesis. 42 (2): 77–85. doi:10.1002/gene.20127. PMID   15864812. S2CID   30511891.
  17. ↑ Dorner AA, Wegmann F, Butz S, Wolburg-Buchholz K, Wolburg H, Mack A, Nasdala I, August B, Westermann J, Rathjen FG, Vestweber D (Aug 2005). "Coxsackievirus-adenovirus receptor (CAR) is essential for early embryonic cardiac development". Journal of Cell Science. 118 (Pt 15): 3509–21. doi: 10.1242/jcs.02476 . PMID   16079292.
  18. 1 2 Chen JW, Zhou B, Yu QC, Shin SJ, Jiao K, Schneider MD, Baldwin HS, Bergelson JM (Apr 2006). "Cardiomyocyte-specific deletion of the coxsackievirus and adenovirus receptor results in hyperplasia of the embryonic left ventricle and abnormalities of sinuatrial valves". Circulation Research. 98 (7): 923–30. doi: 10.1161/01.RES.0000218041.41932.e3 . PMID   16543498.
  19. ↑ Lim BK, Xiong D, Dorner A, Youn TJ, Yung A, Liu TI, Gu Y, Dalton ND, Wright AT, Evans SM, Chen J, Peterson KL, McCulloch AD, Yajima T, Knowlton KU (Aug 2008). "Coxsackievirus and adenovirus receptor (CAR) mediates atrioventricular-node function and connexin 45 localization in the murine heart". The Journal of Clinical Investigation. 118 (8): 2758–70. doi:10.1172/JCI34777. PMC   2467382 . PMID   18636119.
  20. 1 2 3 Marsman RF, Bezzina CR, Freiberg F, Verkerk AO, Adriaens ME, Podliesna S, Chen C, Purfürst B, Spallek B, Koopmann TT, Baczko I, Dos Remedios CG, George AL, Bishopric NH, Lodder EM, de Bakker JM, Fischer R, Coronel R, Wilde AA, Gotthardt M, Remme CA (Feb 2014). "Coxsackie and adenovirus receptor is a modifier of cardiac conduction and arrhythmia vulnerability in the setting of myocardial ischemia". Journal of the American College of Cardiology. 63 (6): 549–59. doi:10.1016/j.jacc.2013.10.062. PMC   3926969 . PMID   24291282.
  21. ↑ Mirza M, Pang MF, Zaini MA, Haiko P, Tammela T, Alitalo K, Philipson L, Fuxe J, Sollerbrant K (2012). "Essential role of the coxsackie- and adenovirus receptor (CAR) in development of the lymphatic system in mice". PLOS ONE. 7 (5): e37523. Bibcode:2012PLoSO...737523M. doi: 10.1371/journal.pone.0037523 . PMC   3356332 . PMID   22624044.
  22. ↑ Bergelson JM, Cunningham JA, Droguett G, Kurt-Jones EA, Krithivas A, Hong JS, Horwitz MS, Crowell RL, Finberg RW (Feb 1997). "Isolation of a common receptor for Coxsackie B viruses and adenoviruses 2 and 5". Science. 275 (5304): 1320–3. doi:10.1126/science.275.5304.1320. PMID   9036860. S2CID   33824689.
  23. ↑ Bowles NE, Richardson PJ, Olsen EG, Archard LC (May 1986). "Detection of Coxsackie-B-virus-specific RNA sequences in myocardial biopsy samples from patients with myocarditis and dilated cardiomyopathy". Lancet. 1 (8490): 1120–3. doi:10.1016/s0140-6736(86)91837-4. PMID   2871380. S2CID   27035726.
  24. ↑ Pauschinger M, Bowles NE, Fuentes-Garcia FJ, Pham V, Kühl U, Schwimmbeck PL, Schultheiss HP, Towbin JA (Mar 1999). "Detection of adenoviral genome in the myocardium of adult patients with idiopathic left ventricular dysfunction". Circulation. 99 (10): 1348–54. doi: 10.1161/01.cir.99.10.1348 . PMID   10077520.
  25. ↑ Andréoletti L, Ventéo L, Douche-Aourik F, Canas F, Lorin de la Grandmaison G, Jacques J, Moret H, Jovenin N, Mosnier JF, Matta M, Duband S, Pluot M, Pozzetto B, Bourlet T (Dec 2007). "Active Coxsackieviral B infection is associated with disruption of dystrophin in endomyocardial tissue of patients who died suddenly of acute myocardial infarction". Journal of the American College of Cardiology. 50 (23): 2207–14. doi: 10.1016/j.jacc.2007.07.080 . PMID   18061067.
  26. ↑ Marsman RF, Wilde AA, Bezzina CR (Feb 2011). "Genetic predisposition for sudden cardiac death in myocardial ischaemia: the Arrhythmia Genetics in the NEtherlandS study". Netherlands Heart Journal. 19 (2): 96–100. doi:10.1007/s12471-010-0070-4. PMC   3040308 . PMID   21461030.
  27. ↑ Bezzina CR, Pazoki R, Bardai A, Marsman RF, de Jong JS, Blom MT, Scicluna BP, Jukema JW, Bindraban NR, Lichtner P, Pfeufer A, Bishopric NH, Roden DM, Meitinger T, Chugh SS, Myerburg RJ, Jouven X, Kääb S, Dekker LR, Tan HL, Tanck MW, Wilde AA (Aug 2010). "Genome-wide association study identifies a susceptibility locus at 21q21 for ventricular fibrillation in acute myocardial infarction". Nature Genetics. 42 (8): 688–91. doi:10.1038/ng.623. PMC   3966292 . PMID   20622880.
  28. ↑ Chopra N, Knollmann BC (May 2011). "Genetics of sudden cardiac death syndromes". Current Opinion in Cardiology. 26 (3): 196–203. doi:10.1097/HCO.0b013e3283459893. PMC   3145336 . PMID   21430528.
  29. ↑ Cohen CJ, Shieh JT, Pickles RJ, Okegawa T, Hsieh JT, Bergelson JM (Dec 2001). "The coxsackievirus and adenovirus receptor is a transmembrane component of the tight junction". Proceedings of the National Academy of Sciences of the United States of America. 98 (26): 15191–6. Bibcode:2001PNAS...9815191C. doi: 10.1073/pnas.261452898 . PMC   65005 . PMID   11734628.

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