{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gonzalez-Gonzalez L"],"funding":["Consejo Nacional de Ciencia y Tecnología","Fundación Miguel Alemán, A.C","SEP-CINVESTAV"],"pagination":["1994351"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9067463"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(2)"],"pubmed_abstract":["ZO-2 is a peripheral <u>t</u>ight <u>j</u>unction (TJ) protein whose silencing in renal epithelia induces cell hypertrophy. Here, we found that in ZO-2 KD MDCK cells, in compensatory renal hypertrophy triggered in rats by a unilateral nephrectomy and in liver steatosis of <u>o</u>bese <u>Z</u>ucker (OZ) rats, ZO-2 silencing is accompanied by the diminished activity of LATS, a kinase of the Hippo pathway, and the nuclear concentration of YAP, the final effector of this signaling route. ZO-2 appears to function as a scaffold for the Hippo pathway as it associates to LATS1. ZO-2 silencing in hypertrophic tissue is due to a diminished abundance of ZO-2 mRNA, and the Sp1 transcription factor is critical for ZO-2 transcription in renal cells. Treatment of OZ rats with metformin, an activator of "],"journal":["Tissue barriers"],"pubmed_title":["ZO-2 favors Hippo signaling, and its re-expression in the steatotic liver by AMPK restores junctional sealing."],"pmcid":["PMC9067463"],"funding_grant_id":["2018","FORDECYT-PRONACES-140644/2020","FIDSC2018/33"],"pubmed_authors":["Alvarez-Salas LM","Garay E","Gallego-Gutierrez H","Hernandez-Guzman C","Rangel-Guerrero SI","Gonzalez-Gonzalez L","Avelino-Cruz JE","Gutierrez-Ruiz MC","Martin-Tapia D","Lopez-Bayghen E","Hernandez-Melchor D","Gonzalez-Mariscal L","Chavez-Munguia B"],"additional_accession":[]},"is_claimable":false,"name":"ZO-2 favors Hippo signaling, and its re-expression in the steatotic liver by AMPK restores junctional sealing.","description":"ZO-2 is a peripheral <u>t</u>ight <u>j</u>unction (TJ) protein whose silencing in renal epithelia induces cell hypertrophy. Here, we found that in ZO-2 KD MDCK cells, in compensatory renal hypertrophy triggered in rats by a unilateral nephrectomy and in liver steatosis of <u>o</u>bese <u>Z</u>ucker (OZ) rats, ZO-2 silencing is accompanied by the diminished activity of LATS, a kinase of the Hippo pathway, and the nuclear concentration of YAP, the final effector of this signaling route. ZO-2 appears to function as a scaffold for the Hippo pathway as it associates to LATS1. ZO-2 silencing in hypertrophic tissue is due to a diminished abundance of ZO-2 mRNA, and the Sp1 transcription factor is critical for ZO-2 transcription in renal cells. Treatment of OZ rats with metformin, an activator of ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2026-04-08T10:05:46.008Z","creation":"2025-04-21T14:49:46.013Z"},"accession":"S-EPMC9067463","cross_references":{"pubmed":["34689705"],"doi":["10.1080/21688370.2021.1994351"]}}