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10.1242/jcs.118703

http://scihub22266oqcxt.onion/10.1242/jcs.118703
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C4342576!4342576!25588839
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suck abstract from ncbi


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pmid25588839      J+Cell+Sci 2015 ; 128 (5): 853-62
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  • IQGAP1 controls tight junction formation through differential regulation of claudin recruitment #MMPMID25588839
  • Tanos BE; Perez Bay AE; Salvarezza S; Vivanco I; Mellinghoff I; Osman M; Sacks DB; Rodriguez-Boulan E
  • J Cell Sci 2015[Mar]; 128 (5): 853-62 PMID25588839show ga
  • IQGAP1 is a scaffolding protein previously implicated in adherens junction formation. However, its role in the establishment or maintenance of tight junctions (TJs) has not been explored. We hypothesized that IQGAP1 could regulate TJ formation by modulating the expression and/or localization of junctional proteins, and we systematically tested this hypothesis in the model Madin-Darby canine kidney (MDCK) cell line. We find that IQGAP1 silencing enhances a transient increase in transepithelial electrical resistance (TER) observed during the early stages of TJ formation (Cereijido et al., 1978). Quantitative microscopy and biochemical experiments suggest that this effect of IQGAP1 on TJ assembly is accounted for by reduced expression and TJ recruitment of claudin 2, and increased TJ recruitment of claudin 4. Furthermore, we show that IQGAP1 also regulates TJ formation through its interactor CDC42, because IQGAP1 knockdown increases the activity of the CDC42 effector JNK and dominant-negative CDC42 prevents the increase in TER caused by IQGAP1 silencing. Hence, we provide evidence that IQGAP1 modulates TJ formation by a twofold mechanism: (1) controlling the expression and recruitment of claudin 2 and recruitment of claudin 4 to the TJ, and (2) transient inhibition of the CDC42?JNK pathway.
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