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. Author manuscript; available in PMC: 2018 Jul 20.
Published in final edited form as: Cell Commun Adhes. 2014 Apr 28;21(3):169–179. doi: 10.3109/15419061.2014.908853

Table I.

Genetic manipulation of adherens junction proteins in the adult myocardium

Mouse model Stress Cardiac Phenotype Reference
N-cadherin LOF None Cardiomyopathy, GJ remodeling, arrhythmia, SCD (Cheng et al., 2011, Franceschini et al., 2013, Kostetskii et al., 2005, Li et al., 2005)
N-cadherin HET PS Normal cardiac function, GJ remodeling, inducible arrhythmia (Li et al., 2008)
β-catenin LOF None Normal cardiac function, increase PG (Zhou et al., 2007)
β-catenin LOF TAC Block hypertrophy, decrease Wnt genes (Chen et al., 2006)
β-catenin LOF AngII No change in hypertrophy response (Baurand et al., 2007)
β-catenin LOF MI Improve LV function, increase cpc (Zelarayan et al., 2008)
β-catenin HET TAC Block hypertrophy, increase fetal genes (Qu et al., 2007)
β-cateninΔex3 GOF None Cardiomyopathy, no change Wnt genes (Hirschy et al., 2010)
β-cateninΔex3 GOF MI No improvement in LV function, decrease cpc differentiation (Zelarayan et al., 2008)
β-cateninΔex3 GOF AngII Block hypertrophy, decrease cardiac function (Baurand et al., 2007)
PG LOF None AC-like pathology except adipocytes (Li et al., 2011a, Li et al., 2011b)
PG Hypomorph None Normal cardiac function, increase β-catenin (Swope et al., 2012)
PG GOF None AC-like pathology including adipocytes (Lombardi et al., 2011)
PGNaxos GOF None AC-like pathology including adipocytes (Lombardi et al., 2011)
αE-catenin LOF None Cardiomyopathy late onset (Sheikh et al., 2006)
αE-catenin LOF MI Ventricular wall rupture (Sheikh et al., 2006)
αT-catenin LOF None Cardiomyopathy early onset, GJ remodeling (Li et al., 2012)
αT-catenin LOF I/R Arrhythmia (Li et al., 2012)

LOF, loss-of-function; GOF, gain-of-function; HET, heterozygous; SCD, sudden cardiac death; PS; program stimulation; GJ, gap junction; TAC, transverse aortic constriction; AngII, angiotensinII; MI, myocardial infarction; cpc, cardiac progenitor cells; I/R, ischemia/reperfusion.