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Biochemistry and microscopy approaches in T cells confirmed SNX27/ZO-2 PDZ-dependent interaction, and demonstrated its role controlling the dynamic localization of ZO-2 at the IS
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A likely causal mutation was identified in the majority (61%), spanning many genes including ones that have only rarely been reported to cause cholestatic liver disease, e.g. TJP2 and VIPAS39
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Patients with a confirmed ABCB11 or tight junction protein 2 gene mutation (n = 7) had a minimally detectable THBA proportion (0.23-2.99% of total BAs). Three patients with an ATP8B1 mutation had an elevated THBA proportion (7.51-37.26%).
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Studies indicate the modular and supramodular organization of zonula occludens protein 2 (ZO-2) that allows it to interact with a wide variety of molecules, including cell-cell adhesion proteins, cytoskeletal components, and nuclear factors.
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Data identified two Disease-causing Genes TJP2 and GJB2 in a Chinese Family with Unconditional Autosomal Dominant Nonsyndromic Hereditary Hearing Impairment.
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TJP2 deficiency may predispose to hepatocellular carcinoma in early childhood
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Claudin-19, the most abundant claudin in myelin, exhibited no binding to ZO2.
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JAM-A regulates epithelial permeability via association with ZO-2, afadin, and PDZ-GEF1 to activate Rap2c and control contraction of the apical cytoskeleton.
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Protein-truncating mutations in the tight junction protein 2 gene cause failure of protein localization and disruption of tight-junction structure, leading to severe cholestatic liver disease.
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demonstrated that ZO-2 inhibition increases invasive and migrative capacities of invasive tumor cells. This was associated with an increase of MT1-MMP
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the Alu-related transcript of TJP2 gene (TJP2-Alu transcript) was differentially expressed between colorectal tumor and normal tissues; potential diagnostic markers for colorectal cancer.
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ZO-2 inhibits the Wnt signaling pathway, reduces cell proliferation, and promotes apoptosis; its absence, mutation, or overexpression is present in various human diseases, including deafness and cancer.
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AmotL1 and ZO-2 are two candidates that could be harnessed to control the oncogenic function of YAP.
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these findings imply involvement of the ZO-2 tight junction independent signaling complex containing Jak1 and uPAR in VSMC intercellular communications.
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ZO-2 interacts with YAP2 to form complex; ZO-2 facilitates both nuclear translocation of YAP2 & pro-apoptotic function of YAP2; YAP2/ZO-2 complex appears to be involved in cell detachment
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The identification of ZASP helps to unfold the complex nuclear molecular arrays that form on ZO-2 scaffolds.
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the first PDZ domain of zona occludens-1 (ZO-1) and 2 (ZO-2) interacts with the carboxy-terminal PDZ binding motif of TAZ
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TJP2- and GSK-3beta-mediated increased susceptibility to apoptosis of cells of the inner ear is the mechanism for adult-onset hearing loss in this kindred and may serve as one model for age-related hearing loss in the general population.
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Study shows that ZO isoforms bind PtdInsPs and offers an alternative regulatory mechanism for the formation and stabilisation of protein complexes in the nucleus.
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Familial hypercholanemia in Amish individuals is associated with mutations in tight junction protein 2 (encoded by TJP2, also known as ZO-2) and bile acid Coenzyme A: amino acid N-acyltransferase (encoded by BAAT).
