Table 2 Mouse models where tight junction-integral or -associated proteins have been genetically manipulated to assess impact on mucosal homeostasis and susceptibility to experimental colitis

Claudin-1

Villin promoter-driven overexpression

Susceptible to experimentally induced colitis^{17, 65, 115}

Proliferation

Migration

Coreceptor

For hepatitis C virus

↑

Colon cancer promotion, coreceptor for hepatitis C, helps in antigen sampling by dendritic cells

Claudin-2

Villin promoter-driven overexpression or homozygous-knockout

Increased gut permeability and immune compensation Resistance to experimentally induced colitis in overexpressing mice

Knockout mice are susceptible to experimentally induced colitis^{15, 48, 53}

Proliferation

Migration

↑

Colon cancer promotion

Claudin-7

Homozygous-knockout or Villin-cre-mediated knockout

Increased gut permeability, spontaneous mucosal inflammation^{63, 66, 116}

Proliferation

Migration

Cell–matrix adhesion

↓

↑

Colon cancer suppressive

JAM-A

Homozygous knockout

Increased gut permeability; immune compensation; resistance to DSS-colitis-induced epithelial injury^{16, 113}

Proliferation

Migration

↓

Promotes epithelial injury repair in mice subjected to DSS-colitis

Occludin

Homozygous knockout

Chronic gastritis^{40, 117}

Proliferation

↓

Decreased expression in IBD and cancer

Myosin light chain kinase

Villin promoter-driven overexpression

Increased mucosal permeability; susceptible to experimentally induced colitis^{10, 41}

Migration

↓

Induces diarrhea

Dominant-negative N-cadherin mutant (delta)

Villin promoter-driven overexpression

Spontaneous mucosal inflammation¹¹

Proliferation

Migration

Cell adhesion

↑

↓

Colon cancer promotion

P120-catenin

Villin-cre-mediated knockout

Spontaneous mucosal inflammation³⁹

Proliferation

Migration

Cell Adhesion

↑

↓

Colon cancer promotion