{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T14:43:50Z","timestamp":1791211430152,"version":"4.1.0"},"reference-count":45,"publisher":"Rockefeller University Press","issue":"1","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2006,10,9]]},"abstract":"<jats:p>Focal adhesion kinase family interacting protein of 200 kD (FIP200) has been shown to regulate diverse cellular functions such as cell size, proliferation, and migration in vitro. However, the function of FIP200 in vivo has not been investigated. We show that targeted deletion of FIP200 in the mouse led to embryonic death at mid\/late gestation associated with heart failure and liver degeneration. We found that FIP200 knockout (KO) embryos show reduced S6 kinase activation and cell size as a result of increased tuberous sclerosis complex function. Furthermore, FIP200 KO embryos exhibited significant apoptosis in heart and liver. Consistent with this, FIP200 KO mouse embryo fibroblasts and liver cells showed increased apoptosis and reduced c-Jun N-terminal kinase phosphorylation in response to tumor necrosis factor (TNF) \u03b1 stimulation, which might be mediated by FIP200 interaction with apoptosis signal\u2013regulating kinase 1 (ASK1) and TNF receptor\u2013associated factor 2 (TRAF2), regulation of TRAF2\u2013ASK1 interaction, and ASK1 phosphorylation. Together, our results reveal that FIP200 functions as a regulatory node to couple two important signaling pathways to regulate cell growth and survival during mouse embryogenesis.<\/jats:p>","DOI":"10.1083\/jcb.200604129","type":"journal-article","created":{"date-parts":[[2006,10,3]],"date-time":"2006-10-03T00:26:25Z","timestamp":1159835185000},"page":"121-133","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":224,"title":["Role of FIP200 in cardiac and liver development and its regulation of TNF\u03b1 and TSC\u2013mTOR signaling pathways"],"prefix":"10.1083","volume":"175","author":[{"given":"Boyi","family":"Gan","sequence":"first","affiliation":[{"name":"1Department of Molecular Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xu","family":"Peng","sequence":"additional","affiliation":[{"name":"1Department of Molecular Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamas","family":"Nagy","sequence":"additional","affiliation":[{"name":"1Department of Molecular Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana","family":"Alcaraz","sequence":"additional","affiliation":[{"name":"2Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Gu","sequence":"additional","affiliation":[{"name":"3Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852"},{"name":"4Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun-Lin","family":"Guan","sequence":"additional","affiliation":[{"name":"1Department of Molecular Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2006,10,2]]},"reference":[{"key":"2023072907513605700_BIB1","doi-asserted-by":"crossref","first-page":"3178","DOI":"10.1091\/mbc.e02-05-0295","volume":"13","year":"2002","journal-title":"Mol. 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