Wikipedia

Plakoglobin

Plakoglobin,also known asjunction plakoglobinorgamma-catenin,is aproteinthat in humans is encoded by theJUPgene.[5]Plakoglobin is a member of thecateninprotein family and homologous toβ-catenin.Plakoglobin is acytoplasmiccomponent ofdesmosomesandadherens junctionsstructures located withinintercalated discsofcardiac musclethat function to anchorsarcomeresand join adjacent cells incardiac muscle.Mutations in plakoglobin are associated witharrhythmogenic right ventricular dysplasia.

JUP
Available structures
PDBOrtholog search:PDBeRCSB
Identifiers
AliasesJUP,ARVD12, CTNNG, DP3, DPIII, PDGB, PKGB, Plakoglobin, junction plakoglobin, PG
External IDsOMIM:173325;MGI:96650;HomoloGene:1680;GeneCards:JUP;OMA:JUP - orthologs
Orthologs
SpeciesHumanMouse
Entrez

3728

16480

Ensembl

ENSG00000173801

ENSMUSG00000001552

UniProt

P14923

Q02257

RefSeq (mRNA)

NM_010593

RefSeq (protein)

NP_034723

Location (UCSC)Chr 17: 41.75 – 41.79 MbChr 11: 100.26 – 100.29 Mb
PubMedsearch[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Structure

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Human plakoglobin is 81.7 kDa in molecular weight and 745 amino acids long.[6]TheJUPgene contains 13 exons spanning 17 kb on chromosome 17q21.[7]Plakoglobin is a member of thecateninfamily, since it contains a distinct repeating amino acid motif called thearmadillo repeat.[5]Plakoglobin is highly similar toβ-catenin;both have 12armadillo repeatsas well asN-terminalandC-terminalglobular domains of unknown structure.[8]Plakoglobin was originally identified as a component ofdesmosomes,where it can bind to thecadherinfamily memberdesmoglein I.Plakoglobin also associates with classical cadherins such asE-cadherin;in that context, it was called gamma-catenin.Plakoglobin forms distinct complexes withcadherinsanddesmosomal cadherins.

Function

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Plakoglobin is a majorcytoplasmiccomponent of bothdesmosomesandadherens junctions,and is the only known constituent common to submembranous plaques in both of these structures,[9]which are located at the intercalated disc (ICD) of cardiomyocytes. Plakoglobin linkscadherinsto theactincytoskeleton.Plakoglobin binds to conserved regions ofdesmogleinanddesmocollinatintracellularcatenin-binding sites to assembledesmosomes.[10][11]

Plakoglobin is essential for normal development ofintercalated discsand stability ofcardiac muscle.Transgenic mice homozygous for a null mutation of theJUPgene die around embryonic day 12 from substantial defects inadherens junctionsand a lack of functional desmosomes in the heart.[12][13]Further studies showed thatcardiacfibers obtained fromJUP-null embryonic mice had decreased passive compliance albeit normal attachment ofsarcomerestoadherens junctions.[14]

In additional studies, an induciblecardiac-specific plakoglobin knockout mice were generated. Transgenic mice displayed a similar phenotype asarrhythmogenic right ventricular cardiomyopathypatients, with loss ofcardiomyocytes,fibrosisand cardiac dysfunction, as well as alterations indesmosomeprotein content andgap junctionremodeling. Hearts also exhibited increases inβ-cateninsignaling.[15][16]Further investigations on the role ofβ-cateninand plakoglobin in the heart generated a double knockout of these two proteins. Mice exhibitedcardiomyopathy,fibrosis,conduction abnormalities andsudden cardiac death,presumably via spontaneous lethal ventriculararrhythmias.Mice also showed a decrease ingap junctionstructures atintercalated discs.[17]

Intracellular plakoglobin expression is controlled byWntsignaling and ubiquitin-proteasome-dependent degradation.PhosphorylationofN-terminalSerinesby a “destruction complex” composed ofglycogen synthase kinase 3β (GSK3β)and scaffold proteinsadenomatous polyposis coli(APC) andaxintargets plakoglobin for degradation.[18][19][20][31–33]. Thephosphorylatedmotif is recognized by β-TrCP, a ubiquitin ligase that targets plakoglobin 26S proteasome-dependent degradation.[21]Plakoglobin is alsoO-glycosylatednear itsN-terminaldestruction box.

Clinical significance

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Mutation of theJUPgene encoding plakoglobin has been implicated as one of the causes of thecardiomyopathyknown asarrhythmogenic right ventricular dysplasia(ARVD) orarrhythmogenic right ventricular cardiomyopathy;mutations inJUPspecifically causes anautosomal recessiveform referred to asNaxos disease.[22][23][24]This form of was first identified in a small cluster of families on the Greek island ofNaxos.The phenotype of theNaxos diseasevariant ofARVDis unique in that it involves the hair and skin as well as the rightventricle.Affected individuals have kinky,wooly hair;there is also palmar and plantarerythemaat birth that progresses tokeratosisas the palms and soles of the feet are used in crawling and walking.[25][26][27]These findings co-segregate 100% with the development ofARVDby early adolescence.

It has become clear thatARVD/ARVCis a disease of thecardiac muscledesmosome;advances in molecular genetics have illuminated this notion.[28][29][30][31][32][33][34][35][36]

Studies investigating the role of plakoglobin in disease pathology have found that suppression ofdesmoplakinexpression bysiRNAled to thenuclearlocalization of plakoglobin, resulting in a reduction inWntsignaling via Tcf/Lef1 and ensued pathogenesis of ARVC.[37]Specifically, adipogenic factor expression was induced and cardiac progenitor cells at the epicardium were differentiated to adipocytes.[38]

Non-invasivecardiacscreening identified T-wave inversion, abnormalities in rightventricularwall motion, and frequent ventricular extrasystoles as sensitive and specific markers of aJUPmutation.[39]Additional studies have shown that immunohistochemical analysis ofcardiac muscledesmosomalproteins is also a sensitive and specific diagnostic text forARVD/ARVC.[40]

Abnormal distribution of plakoglobin due to mutations in genes encoding forDesmoglein1 and 3 have also been implicated inPemphigus vulgaris.[41][42]

Interactions

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Plakoglobin has been shown tointeractwith:

See also

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References

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  1. ^abcGRCh38: Ensembl release 89: ENSG00000173801–Ensembl,May 2017
  2. ^abcGRCm38: Ensembl release 89: ENSMUSG00000001552–Ensembl,May 2017
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  4. ^"Mouse PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
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Further reading

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