{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T20:01:31Z","timestamp":1786132891651,"version":"build-2736575974"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81873597"],"award-info":[{"award-number":["81873597"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81974083"],"award-info":[{"award-number":["81974083"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81370783"],"award-info":[{"award-number":["81370783"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81620108029"],"award-info":[{"award-number":["81620108029"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81330074"],"award-info":[{"award-number":["81330074"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004826","name":"Natural Science Foundation of Beijing Municipality","doi-asserted-by":"publisher","award":["7212151"],"award-info":[{"award-number":["7212151"]}],"id":[{"id":"10.13039\/501100004826","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01-DK-096015"],"award-info":[{"award-number":["R01-DK-096015"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R21-DK-092619"],"award-info":[{"award-number":["R21-DK-092619"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005294","name":"Massachusetts General Hospital","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005294","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100012489","name":"Boston Area Diabetes Endocrinology Research Center","doi-asserted-by":"publisher","award":["DK-57521"],"award-info":[{"award-number":["DK-57521"]}],"id":[{"id":"10.13039\/100012489","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Center for the Study of Inflammatory Bowel Disease","award":["DK43351"],"award-info":[{"award-number":["DK43351"]}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2021,9]]},"abstract":"<jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>Focal adhesion kinase (FAK) has been widely studied and shown to have a crucial effect on tumor progression. Although autosomal dominant polycystic kidney disease (ADPKD) shares numerous commonalities with tumors, it is undetermined whether FAK is involved in cyst development. Our study demonstrates that inhibiting FAK activity using small molecule FAK inhibitor VS-4718 ameliorates ADPKD progression and improves renal function. Inhibiting FAK and its downstream Src signaling suppresses cAMP-mediated aberrant proliferation of cystic epithelial cells in ADPKD animals. This study highlights the therapeutic potential of small molecule FAK inhibitors in treating patients with ADPKD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Autosomal dominant polycystic kidney disease (ADPKD) is characterized by numerous cysts originating from renal tubules and is associated with significant tubular epithelial cell proliferation. Focal adhesion kinase (FAK) promotes tumor growth by regulating multiple proliferative pathways.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We established the forskolin (FSK)-induced three-dimensional (3D) Madin\u2013Darby Canine Kidney cystogenesis model and 8-bromoadenosine-3`,5`-cyclic monophosphate\u2013stimulated cyst formation in\n                      <jats:italic toggle=\"yes\">ex vivo<\/jats:italic>\n                      embryonic kidney culture. Cultured human renal cyst\u2013lining cells (OX-161) and normal tubular epithelial cells were treated with FAK inhibitors or transfected with green fluorescent protein\u2013tagged FAK mutant plasmids for proliferation study. Furthermore, we examined the role of FAK in two transgenic ADPKD animal models, the kidney-specific\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      knockout and the collecting duct\u2013specific\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      knockout mouse models.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      FAK activity was significantly elevated in OX-161 cells and in two ADPKD mouse models. Inhibiting FAK activity reduced cell proliferation in OX-161 cells and prevented cyst growth in\n                      <jats:italic toggle=\"yes\">ex vivo<\/jats:italic>\n                      and 3D cyst models. In tissue-specific\n                      <jats:italic toggle=\"yes\">Pkd1<\/jats:italic>\n                      knockout mouse models, FAK inhibitors retarded cyst development and mitigated renal function decline. Mechanically, FSK stimulated FAK activation in tubular epithelial cells, which was blocked by a protein kinase A (PKA) inhibitor. Inhibition of FAK activation by inhibitors or transfected cells with mutant FAK constructs interrupted FSK-mediated Src activation and upregulation of ERK and mTOR pathways.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our study demonstrates the critical involvement of FAK in renal cyst development, suggests that FAK is a potential therapeutic target in treating patients with ADPKD, and highlights the role of FAK in cAMP-PKA\u2013regulated proliferation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2020111560","type":"journal-article","created":{"date-parts":[[2021,8,31]],"date-time":"2021-08-31T15:25:18Z","timestamp":1630423518000},"page":"2159-2174","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":15,"title":["Inhibiting Focal Adhesion Kinase Ameliorates Cyst Development in Polycystin-1\u2013Deficient Polycystic Kidney Disease in Animal Model"],"prefix":"10.1681","volume":"32","clinical-trial-number":[{"clinical-trial-number":"nct01849744","registry":"10.18810\/clinical-trials-gov"},{"clinical-trial-number":"nct02428270","registry":"10.18810\/clinical-trials-gov"},{"clinical-trial-number":"nct01951690","registry":"10.18810\/clinical-trials-gov"}],"author":[{"given":"Jinzhao","family":"He","sequence":"first","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"},{"name":"Center for Systems Biology, Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shun","family":"Zhang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiwei","family":"Qiu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaowei","family":"Li","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huihui","family":"Huang","sequence":"additional","affiliation":[{"name":"Center for Systems Biology, Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts"},{"name":"Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7402-0360","authenticated-orcid":false,"given":"William","family":"Jin","sequence":"additional","affiliation":[{"name":"Division of Graduate Medical Sciences, Boston University School of Medicine, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yue","family":"Xu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guangying","family":"Shao","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liang","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia","family":"Meng","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuyuan","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoqiang","family":"Geng","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yingli","family":"Jia","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Li","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"},{"name":"Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baoxue","family":"Yang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"},{"name":"Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua A.","family":"Jenny Lu","sequence":"additional","affiliation":[{"name":"Center for Systems Biology, Program in Membrane Biology and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts"},{"name":"Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Zhou","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, China"},{"name":"Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2021,9]]},"reference":[{"key":"B1-20240826","doi-asserted-by":"crossref","first-page":"1004","DOI":"10.1038\/ng.2715","article-title":"Loss of cilia suppresses cyst growth in genetic models of autosomal dominant polycystic kidney disease","volume":"45","author":"Ma","year":"2013","journal-title":"Nat Genet"},{"key":"B2-20240826","doi-asserted-by":"crossref","first-page":"4148","DOI":"10.1038\/s41467-019-11918-y","article-title":"Discovery and preclinical evaluation of anti-miR-17 oligonucleotide RGLS4326 for the treatment of polycystic kidney disease","volume":"10","author":"Lee","year":"2019","journal-title":"Nat Commun"},{"key":"B3-20240826","doi-asserted-by":"crossref","first-page":"151","DOI":"10.1056\/NEJMra022161","article-title":"Polycystic kidney disease","volume":"350","author":"Wilson","year":"2004","journal-title":"N Engl J Med"},{"key":"B4-20240826","doi-asserted-by":"crossref","first-page":"451","DOI":"10.1038\/nrneph.2015.39","article-title":"Vasopressin and disruption of calcium signalling in polycystic kidney disease","volume":"11","author":"Chebib","year":"2015","journal-title":"Nat Rev Nephrol"},{"key":"B5-20240826","doi-asserted-by":"crossref","first-page":"18","DOI":"10.1681\/ASN.2013040398","article-title":"Strategies targeting cAMP signaling in the treatment of polycystic kidney disease","volume":"25","author":"Torres","year":"2014","journal-title":"J Am Soc Nephrol"},{"key":"B6-20240826","doi-asserted-by":"crossref","first-page":"750","DOI":"10.1038\/nrneph.2017.127","article-title":"New treatment paradigms for ADPKD: Moving towards precision medicine","volume":"13","author":"Lanktree","year":"2017","journal-title":"Nat Rev Nephrol"},{"key":"B7-20240826","doi-asserted-by":"crossref","first-page":"112","DOI":"10.1038\/nature13541","article-title":"Endothelial-cell FAK targeting sensitizes tumours to DNA-damaging therapy","volume":"514","author":"Tavora","year":"2014","journal-title":"Nature"},{"key":"B8-20240826","doi-asserted-by":"crossref","first-page":"132","DOI":"10.1016\/j.pharmthera.2014.10.001","article-title":"FAK signaling in human cancer as a target for therapeutics","volume":"146","author":"Lee","year":"2015","journal-title":"Pharmacol Ther"},{"key":"B9-20240826","doi-asserted-by":"crossref","first-page":"610","DOI":"10.1016\/j.addr.2010.11.001","article-title":"Focal adhesion kinase and its signaling pathways in cell migration and angiogenesis","volume":"63","author":"Zhao","year":"2011","journal-title":"Adv Drug Deliv Rev"},{"key":"B10-20240826","doi-asserted-by":"crossref","first-page":"598","DOI":"10.1038\/nrc3792","article-title":"FAK in cancer: Mechanistic findings and clinical applications","volume":"14","author":"Sulzmaier","year":"2014","journal-title":"Nat Rev Cancer"},{"key":"B11-20240826","doi-asserted-by":"crossref","first-page":"1017","DOI":"10.1016\/j.kint.2020.01.026","article-title":"Tenascin-C promotes acute kidney injury to chronic kidney disease progression by impairing tubular integrity via \u03b1v\u03b26 integrin signaling","volume":"97","author":"Zhu","year":"2020","journal-title":"Kidney Int"},{"key":"B12-20240826","doi-asserted-by":"crossref","first-page":"1145","DOI":"10.1681\/ASN.2009090991","article-title":"Inhibition of podocyte FAK protects against proteinuria and foot process effacement","volume":"21","author":"Ma","year":"2010","journal-title":"J Am Soc Nephrol"},{"key":"B13-20240826","doi-asserted-by":"crossref","first-page":"2005","DOI":"10.1046\/j.1523-1755.2001.00716.x","article-title":"Treatment prospects for autosomal-dominant polycystic kidney disease","volume":"59","author":"Qian","year":"2001","journal-title":"Kidney Int"},{"key":"B14-20240826","doi-asserted-by":"crossref","first-page":"1239","DOI":"10.1016\/j.bbadis.2011.05.008","article-title":"Apico-basal polarity in polycystic kidney disease epithelia","volume":"1812","author":"Wilson","year":"2011","journal-title":"Biochim Biophys Acta"},{"key":"B15-20240826","doi-asserted-by":"crossref","first-page":"533","DOI":"10.1159\/000500458","article-title":"Identification of key genes and candidated pathways in human autosomal dominant polycystic kidney disease by bioinformatics analysis","volume":"44","author":"Liu","year":"2019","journal-title":"Kidney Blood Press Res"},{"key":"B16-20240826","doi-asserted-by":"crossref","first-page":"2310","DOI":"10.1681\/ASN.2018010074","article-title":"Interactions between macrophages and cyst-lining epithelial cells promote kidney cyst growth in Pkd1-deficient mice","volume":"29","author":"Yang","year":"2018","journal-title":"J Am Soc Nephrol"},{"key":"B17-20240826","doi-asserted-by":"crossref","first-page":"157","DOI":"10.1038\/sj.ki.5002229","article-title":"Hyperproliferation of PKD1 cystic cells is induced by insulin-like growth factor-1 activation of the Ras\/Raf signalling system","volume":"72","author":"Parker","year":"2007","journal-title":"Kidney Int"},{"key":"B18-20240826","doi-asserted-by":"crossref","first-page":"6185","DOI":"10.1096\/fj.201801338RRR","article-title":"Aquaporin-3 deficiency slows cyst enlargement in experimental mouse models of autosomal dominant polycystic kidney disease","volume":"33","author":"Wang","year":"2019","journal-title":"FASEB J"},{"key":"B19-20240826","doi-asserted-by":"crossref","first-page":"2097","DOI":"10.1681\/ASN.2019020204","article-title":"Gentamicin-induced acute kidney injury in an animal model involves programmed necrosis of the collecting duct","volume":"31","author":"Huang","year":"2020","journal-title":"J Am Soc Nephrol"},{"key":"B20-20240826","doi-asserted-by":"crossref","first-page":"104751","DOI":"10.1016\/j.phrs.2020.104751","article-title":"Cardamonin retards progression of autosomal dominant polycystic kidney disease via inhibiting renal cyst growth and interstitial fibrosis","volume":"155","author":"He","year":"2020","journal-title":"Pharmacol Res"},{"key":"B21-20240826","doi-asserted-by":"crossref","first-page":"342","DOI":"10.1016\/j.jhep.2015.08.036","article-title":"Loss of Gs\u03b1 impairs liver regeneration through a defect in the crosstalk between cAMP and growth factor signaling","volume":"64","author":"Lu","year":"2016","journal-title":"J Hepatol"},{"key":"B22-20240826","doi-asserted-by":"crossref","first-page":"375","DOI":"10.1083\/jcb.201702184","article-title":"Pyk2 and FAK differentially regulate invadopodia formation and function in breast cancer cells","volume":"217","author":"Genna","year":"2018","journal-title":"J Cell Biol"},{"key":"B23-20240826","doi-asserted-by":"crossref","first-page":"735","DOI":"10.1038\/s41581-019-0183-y","article-title":"The pathobiology of polycystic kidney disease from a metabolic viewpoint","volume":"15","author":"Menezes","year":"2019","journal-title":"Nat Rev Nephrol"},{"key":"B24-20240826","doi-asserted-by":"crossref","first-page":"2953","DOI":"10.1038\/s41388-018-0177-4","article-title":"Depression promotes prostate cancer invasion and metastasis via a sympathetic-cAMP-FAK signaling pathway","volume":"37","author":"Cheng","year":"2018","journal-title":"Oncogene"},{"key":"B25-20240826","doi-asserted-by":"crossref","first-page":"3404","DOI":"10.1681\/ASN.2016111232","article-title":"Bosutinib versus placebo for autosomal dominant polycystic kidney disease","volume":"28","author":"Tesar","year":"2017","journal-title":"J Am Soc Nephrol"},{"key":"B26-20240826","doi-asserted-by":"crossref","first-page":"1331","DOI":"10.1681\/ASN.2007060665","article-title":"Src inhibition ameliorates polycystic kidney disease","volume":"19","author":"Sweeney","year":"2008","journal-title":"J Am Soc Nephrol"},{"key":"B27-20240826","doi-asserted-by":"crossref","first-page":"793","DOI":"10.1016\/j.celrep.2019.12.075","article-title":"Periostin promotes colorectal tumorigenesis through integrin-FAK-Src pathway-mediated YAP\/TAZ activation","volume":"30","author":"Ma","year":"2020","journal-title":"Cell Rep"},{"key":"B28-20240826","doi-asserted-by":"crossref","first-page":"64","DOI":"10.1016\/j.ccell.2018.11.016","article-title":"Tinagl1 suppresses triple-negative breast cancer progression and metastasis by simultaneously inhibiting integrin\/FAK and EGFR signaling","volume":"35","author":"Shen","year":"2019","journal-title":"Cancer Cell"},{"key":"B29-20240826","doi-asserted-by":"crossref","first-page":"2018","DOI":"10.1111\/j.1523-1755.2004.00623.x","article-title":"EGF-related growth factors in the pathogenesis of murine ARPKD","volume":"65","author":"MacRae Dell","year":"2004","journal-title":"Kidney Int"},{"key":"B30-20240826","doi-asserted-by":"crossref","first-page":"647","DOI":"10.1016\/j.bbadis.2006.04.006","article-title":"Inhibition of HER-2(neu\/ErbB2) restores normal function and structure to polycystic kidney disease (PKD) epithelia","volume":"1762","author":"Wilson","year":"2006","journal-title":"Biochim Biophys Acta"},{"key":"B31-20240826","doi-asserted-by":"crossref","first-page":"3617","DOI":"10.1172\/JCI41531","article-title":"Failure to ubiquitinate c-Met leads to hyperactivation of mTOR signaling in a mouse model of autosomal dominant polycystic kidney disease","volume":"120","author":"Qin","year":"2010","journal-title":"J Clin Invest"},{"key":"B32-20240826","doi-asserted-by":"crossref","first-page":"e135700","DOI":"10.1172\/jci.insight.135700","article-title":"Metalloproteinase PAPP-A regulation of IGF-1 contributes to polycystic kidney disease pathogenesis","volume":"5","author":"Kashyap","year":"2020","journal-title":"JCI Insight"},{"key":"B33-20240826","doi-asserted-by":"crossref","first-page":"289","DOI":"10.1038\/s41581-020-0260-2","article-title":"Targeting angiogenesis and lymphangiogenesis in kidney disease","volume":"16","author":"Tanabe","year":"2020","journal-title":"Nat Rev Nephrol"},{"key":"B34-20240826","doi-asserted-by":"crossref","first-page":"3049","DOI":"10.1681\/ASN.2006030234","article-title":"Stable knockdown of polycystin-1 confers integrin-alpha2beta1-mediated anoikis resistance","volume":"17","author":"Battini","year":"2006","journal-title":"J Am Soc Nephrol"},{"key":"B35-20240826","doi-asserted-by":"crossref","first-page":"888","DOI":"10.1681\/ASN.2013111179","article-title":"Inactivation of integrin-\u03b21 prevents the development of polycystic kidney disease after the loss of polycystin-1","volume":"26","author":"Lee","year":"2015","journal-title":"J Am Soc Nephrol"},{"key":"B36-20240826","first-page":"1311","article-title":"The PKD1 gene product, \u201cpolycystin-1,\u201d is a tyrosine-phosphorylated protein that colocalizes with alpha2beta1-integrin in focal clusters in adherent renal epithelia","volume":"79","author":"Wilson","year":"1999","journal-title":"Lab Invest"},{"key":"B37-20240826","doi-asserted-by":"crossref","first-page":"F1026","DOI":"10.1152\/ajprenal.00038.2017","article-title":"Deletion of \u03b21-integrin in collecting duct principal cells leads to tubular injury and renal medullary fibrosis","volume":"313","author":"Mamuya","year":"2017","journal-title":"Am J Physiol Renal Physiol"},{"key":"B38-20240826","doi-asserted-by":"crossref","first-page":"2708","DOI":"10.1681\/ASN.2016111235","article-title":"Integrin-linked kinase signaling promotes cyst growth and fibrosis in polycystic kidney disease","volume":"28","author":"Raman","year":"2017","journal-title":"J Am Soc Nephrol"},{"key":"B39-20240826","doi-asserted-by":"crossref","first-page":"515","DOI":"10.1038\/nrneph.2015.46","article-title":"The hallmarks of cancer: Relevance to the pathogenesis of polycystic kidney disease","volume":"11","author":"Seeger-Nukpezah","year":"2015","journal-title":"Nat Rev Nephrol"},{"key":"B40-20240826","doi-asserted-by":"crossref","first-page":"851","DOI":"10.1038\/nm.4123","article-title":"Targeting focal adhesion kinase renders pancreatic cancers responsive to checkpoint immunotherapy","volume":"22","author":"Jiang","year":"2016","journal-title":"Nat Med"},{"key":"B41-20240826","doi-asserted-by":"crossref","first-page":"122","DOI":"10.1136\/gutjnl-2018-317424","article-title":"Development of resistance to FAK inhibition in pancreatic cancer is linked to stromal depletion","volume":"69","author":"Jiang","year":"2020","journal-title":"Gut"},{"key":"B42-20240826","doi-asserted-by":"crossref","first-page":"39","DOI":"10.1007\/s11523-019-00621-z","article-title":"BI 853520, a FAK-simile of prior FAK inhibitors?","volume":"14","author":"Lee","year":"2019","journal-title":"Target Oncol"},{"key":"B43-20240826","doi-asserted-by":"crossref","first-page":"778","DOI":"10.4161\/cbt.9.10.11433","article-title":"Oral delivery of PND-1186 FAK inhibitor decreases tumor growth and spontaneous breast to lung metastasis in pre-clinical models","volume":"9","author":"Walsh","year":"2010","journal-title":"Cancer Biol Ther"},{"key":"B44-20240826","doi-asserted-by":"crossref","first-page":"358","DOI":"10.1016\/j.jpba.2017.11.022","article-title":"LC-ESI-MS\/MS determination of defactinib, a novel FAK inhibitor in mice plasma and its application to a pharmacokinetic study in mice","volume":"149","author":"Hallur","year":"2018","journal-title":"J Pharm Biomed Anal"},{"key":"B45-20240826","doi-asserted-by":"crossref","first-page":"2268","DOI":"10.1093\/annonc\/mdw427","article-title":"A phase I, pharmacokinetic and pharmacodynamic study of GSK2256098, a focal adhesion kinase inhibitor, in patients with advanced solid tumors","volume":"27","author":"Soria","year":"2016","journal-title":"Ann Oncol"},{"key":"B46-20240826","doi-asserted-by":"crossref","first-page":"1236","DOI":"10.3389\/fphar.2018.01236","article-title":"VS-4718 antagonizes multidrug resistance in ABCB1- and ABCG2-overexpressing cancer cells by inhibiting the efflux function of ABC transporters","volume":"9","author":"Ji","year":"2018","journal-title":"Front Pharmacol"},{"key":"B47-20240826","doi-asserted-by":"crossref","first-page":"1551","DOI":"10.2353\/ajpath.2008.080308","article-title":"Mammary epithelial-specific disruption of focal adhesion kinase retards tumor formation and metastasis in a transgenic mouse model of human breast cancer","volume":"173","author":"Provenzano","year":"2008","journal-title":"Am J Pathol"},{"key":"B48-20240826","first-page":"252","article-title":"Ras- and PI3K-dependent breast tumorigenesis in mice and humans requires focal adhesion kinase signaling","volume":"119","author":"Pylayeva","year":"2009","journal-title":"J Clin Invest"},{"key":"B49-20240826","doi-asserted-by":"crossref","first-page":"176","DOI":"10.1016\/S0014-5793(01)02545-5","article-title":"Differential regulation of cell migration and cell cycle progression by FAK complexes with Src, PI3K, Grb7 and Grb2 in focal contacts","volume":"499","author":"Shen","year":"2001","journal-title":"FEBS Lett"},{"key":"B50-20240826","doi-asserted-by":"crossref","first-page":"287","DOI":"10.1002\/ijc.26351","article-title":"The role of focal adhesion kinase catalytic activity on the proliferation and migration of squamous cell carcinoma cells","volume":"131","author":"Serrels","year":"2012","journal-title":"Int J Cancer"},{"key":"B51-20240826","doi-asserted-by":"crossref","first-page":"1485","DOI":"10.1093\/jnci\/djt210","article-title":"Role of focal adhesion kinase in regulating YB-1-mediated paclitaxel resistance in ovarian cancer","volume":"105","author":"Kang","year":"2013","journal-title":"J Natl Cancer Inst"},{"key":"B52-20240826","doi-asserted-by":"crossref","first-page":"259","DOI":"10.1016\/j.devcel.2010.07.015","article-title":"Focal adhesion kinase is required for intestinal regeneration and tumorigenesis downstream of Wnt\/c-Myc signaling","volume":"19","author":"Ashton","year":"2010","journal-title":"Dev Cell"},{"key":"B53-20240826","doi-asserted-by":"crossref","first-page":"60","DOI":"10.1016\/j.lungcan.2019.10.033","article-title":"Phase 2 study of the focal adhesion kinase inhibitor defactinib (VS-6063) in previously treated advanced KRAS mutant non-small cell lung cancer","volume":"139","author":"Gerber","year":"2020","journal-title":"Lung Cancer"}],"container-title":["Journal of the American Society of Nephrology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ovid.com\/10.1681\/ASN.2020111560","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T19:25:33Z","timestamp":1786130733000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ovid.com\/10.1681\/ASN.2020111560"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,9]]},"references-count":53,"journal-issue":{"issue":"9","published-print":{"date-parts":[[2021]]}},"URL":"https:\/\/doi.org\/10.1681\/asn.2020111560","relation":{},"ISSN":["1046-6673","1533-3450"],"issn-type":[{"value":"1046-6673","type":"print"},{"value":"1533-3450","type":"electronic"}],"subject":[],"published":{"date-parts":[[2021,9]]},"assertion":[{"value":"2020-11-03","name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2021-04-07","name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}}]}}