Kai Yu, PhD

"As a developmental biologist, my goal is to translate knowledge gained from animal model studies into clinical treatments of human birth defects. I am particularly interested in cleft palate, one of the most common birth defects. Although cleft palate can be corrected by surgical treatments after birth, patients with cleft palate need multidisciplinary care and follow-up treatment of complications from birth to adulthood. At Seattle Children's, I combine mouse genetics and state-of-the-art three-dimensional imaging technologies to undersatnd palate morphogenesis during embryonic development and to investigate how various genetic and environmental risk factors disturb normal development to cause cleft palate formation. I hope that one day my research will aid in developing new strategies for prevention, diagnosis and treatment of cleft palate disorders."

  • Kai Yu, PhD, is an acting assistant professor in the Department of Pediatrics at the University of Washington School of Medicine and a member of the Seattle Children's Research Institute's Center for Developmental Biology and Regenerative Medicine.

    Dr. Yu, who was trained in Dr. David Ornitz's lab at Washington University School of Medicine, has focused on the function of fibroblast growth factor receptors (FGFRs) in skeletal development and pathogenesis of human craniosynostosis. At Seattle Children's, Dr. Yu's primary research interests focus on molecular, cellular and morphogenetic mechanisms of normal secondary palate morphogenesis and the pathogenesis of cleft palate. He is also investigating molecular and cellular mechanisms of midfacial hypoplasia caused by mutations in FGFRs.

  • Award Name Award Description Awarded By Award Date
    T32 National Research Service Award National Institutes of Health 2002 - 2005
    • Yu K, Ornitz DM
      Histomorphological study of palatal shelf elevation during murine secondary palate formation.
      21618642 Developmental dynamics : an official publication of the American Association of Anatomists , 2011 July : 240(7)1737-44 PMCID: PMC3275090
    • Snyder-Warwick AK, Perlyn CA, Pan J, Yu K, Zhang L, Ornitz DM
      Analysis of a gain-of-function FGFR2 Crouzon mutation provides evidence of loss of function activity in the etiology of cleft palate.
      20133659 Proceedings of the National Academy of Sciences of the United States of America , 2010 Feb. 9 : 107(6)2515-20 PMCID: PMC2823872
    • Zhao H, Yang T, Madakashira BP, Thiels CA, Bechtle CA, Garcia CM, Zhang H, Yu K, Ornitz DM, Beebe DC, Robinson ML
      Fibroblast growth factor receptor signaling is essential for lens fiber cell differentiation.
      18455718 Developmental biology , 2008 June 15 : 318(2)276-88 PMCID: PMC2574794
    • Yu K, Ornitz DM
      FGF signaling regulates mesenchymal differentiation and skeletal patterning along the limb bud proximodistal axis.
      18094024 Development (Cambridge, England) , 2008 Feb. : 135(3)483-91
    • Saarimäki-Vire J, Peltopuro P, Lahti L, Naserke T, Blak AA, Vogt Weisenhorn DM, Yu K, Ornitz DM, Wurst W, Partanen J
      Fibroblast growth factor receptors cooperate to regulate neural progenitor properties in the developing midbrain and hindbrain.
      17687036 The Journal of neuroscience : the official journal of the Society for Neuroscience , 2007 Aug. 8 : 27(32)8581-92
    • Hung IH, Yu K, Lavine KJ, Ornitz DM
      FGF9 regulates early hypertrophic chondrocyte differentiation and skeletal vascularization in the developing stylopod.
      17544391 Developmental biology , 2007 July 15 : 307(2)300-13 PMCID: PMC2267922
    • Lin Y, Liu G, Zhang Y, Hu YP, Yu K, Lin C, McKeehan K, Xuan JW, Ornitz DM, Shen MM, Greenberg N, McKeehan WL, Wang F
      Fibroblast growth factor receptor 2 tyrosine kinase is required for prostatic morphogenesis and the acquisition of strict androgen dependency for adult tissue homeostasis.
      17215304 Development (Cambridge, England) , 2007 Feb. : 134(4)723-34
    • Kaga Y, Shoemaker WJ, Furusho M, Bryant M, Rosenbluth J, Pfeiffer SE, Oh L, Rasband M, Lappe-Siefke C, Yu K, Ornitz DM, Nave KA, Bansal R
      Mice with conditional inactivation of fibroblast growth factor receptor-2 signaling in oligodendrocytes have normal myelin but display dramatic hyperactivity when combined with Cnp1 inactivation.
      17122059 The Journal of neuroscience : the official journal of the Society for Neuroscience , 2006 Nov. 22 : 26(47)12339-50
    • Gutin G, Fernandes M, Palazzolo L, Paek H, Yu K, Ornitz DM, McConnell SK, Hébert JM
      FGF signalling generates ventral telencephalic cells independently of SHH.
      16818446 Development (Cambridge, England) , 2006 Aug. : 133(15)2937-46
    • McDowell LM, Frazier BA, Studelska DR, Giljum K, Chen J, Liu J, Yu K, Ornitz DM, Zhang L
      Inhibition or activation of Apert syndrome FGFR2 (S252W) signaling by specific glycosaminoglycans.
      16373332 The Journal of biological chemistry , 2006 Mar. 17 : 281(11)6924-30
    • Wang Y, Xiao R, Yang F, Karim BO, Iacovelli AJ, Cai J, Lerner CP, Richtsmeier JT, Leszl JM, Hill CA, Yu K, Ornitz DM, Elisseeff J, Huso DL, Jabs EW
      Abnormalities in cartilage and bone development in the Apert syndrome FGFR2(+/S252W) mouse.
      15975938 Development (Cambridge, England) , 2005 Aug. : 132(15)3537-48
    • Garcia CM, Yu K, Zhao H, Ashery-Padan R, Ornitz DM, Robinson ML, Beebe DC
      Signaling through FGF receptor-2 is required for lens cell survival and for withdrawal from the cell cycle during lens fiber cell differentiation.
      15778993 Developmental dynamics : an official publication of the American Association of Anatomists , 2005 June : 233(2)516-27
    • White KE, Cabral JM, Davis SI, Fishburn T, Evans WE, Ichikawa S, Fields J, Yu X, Shaw NJ, McLellan NJ, McKeown C, Fitzpatrick D, Yu K, Ornitz DM, Econs MJ
      Mutations that cause osteoglophonic dysplasia define novel roles for FGFR1 in bone elongation.
      15625620 American journal of human genetics , 2005 Feb. : 76(2)361-7 PMCID: PMC1196382
    • Hu H, Hilton MJ, Tu X, Yu K, Ornitz DM, Long F
      Sequential roles of Hedgehog and Wnt signaling in osteoblast development.
      15576404 Development (Cambridge, England) , 2005 Jan. : 132(1)49-60
    • Lavine KJ, Yu K, White AC, Zhang X, Smith C, Partanen J, Ornitz DM
      Endocardial and epicardial derived FGF signals regulate myocardial proliferation and differentiation in vivo.
      15621532 Developmental cell , 2005 Jan. : 8(1)85-95
    • Bialek P, Kern B, Yang X, Schrock M, Sosic D, Hong N, Wu H, Yu K, Ornitz DM, Olson EN, Justice MJ, Karsenty G
      A twist code determines the onset of osteoblast differentiation.
      15030764 Developmental cell , 2004 Mar. : 6(3)423-35
    • Yu K, Xu J, Liu Z, Sosic D, Shao J, Olson EN, Towler DA, Ornitz DM
      Conditional inactivation of FGF receptor 2 reveals an essential role for FGF signaling in the regulation of osteoblast function and bone growth.
      12756187 Development (Cambridge, England) , 2003 July : 130(13)3063-74
    • oi D, Richardson JA, Yu K, Ornitz DM, Olson EN
      Twist regulates cytokine gene expression through a negative feedback loop that represses NF-kappaB activity.
      12553906 Cell , 2003 Jan. 24 : 112(2)169-80
    • Ibrahimi OA, Eliseenkova AV, Plotnikov AN, Yu K, Ornitz DM, Mohammadi M
      Structural basis for fibroblast growth factor receptor 2 activation in Apert syndrome.
      11390973 Proceedings of the National Academy of Sciences of the United States of America , 2001 June 19 : 98(13)7182-7 PMCID: PMC34643
    • Yu K, Ornitz DM
      Uncoupling fibroblast growth factor receptor 2 ligand binding specificity leads to Apert syndrome-like phenotypes.
      11274381 Proceedings of the National Academy of Sciences of the United States of America , 2001 Mar. 27 : 98(7)3641-3 PMCID: PMC33332
    • Yu K, Herr AB, Waksman G, Ornitz DM
      Loss of fibroblast growth factor receptor 2 ligand-binding specificity in Apert syndrome.
      11121055 Proceedings of the National Academy of Sciences of the United States of America , 2000 Dec. 19 : 97(26)14536-41 PMCID: PMC18954