IndraLab

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ANG translocates to the cytoplasm. 6 / 6
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"Given the facts that phosphorylation of VE-cadherin was enhanced and endocytosis of disassembled VE-cadherin increased when cytoplasmic translocation of exogenous ANG took place, we conclude that, in addition to its angiogenic role, ANG is a key enhancing factor on endothelial barrier dysfunction."
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"As a stress activated and secreted ribonuclease, ANG can be transported to the cytoplasm under stress conditions."
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"By investigating the function and potential effects of this compartmentalized translocation of ANG, we found that rickettisial infection-triggered cytoplasmic translocation of ANG, enhanced phosphorylation of VE-cadherin, reduced VE-cadherin stability, and attenuated endothelial barrier function."
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"Most importantly, ANG was translocated into the cytoplasm at 48 hrs p.i. (Figure  xref K) and predominated in the cytoplasmic location at 72 hrs p.i. (Figure  xref L)."
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"However, there is no direct evidence of cytoplasmic translocation of ANG in endothelial cells triggered by adverse events [ xref ]."
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"The mechanism by which SFG rickettsial infection-triggered cytoplasmic translocation of ANG results in phosphorylation of VE-cadherin mediated endothelial barrier dysfunction has yet to be determined."
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