Kathleen K. Sulik, Ph.D.


Lab Personnel


  • B.S., Drake University, 1970
  • Ph.D., University of Tennessee, 1976
  • Postdoc, UNC-Chapel Hill, 1976-78
  • Joined the Department in 1980

Funding Sources

  • National Institutes of Health

Research Interests

Research in the Sulik laboratory is directed toward achieving a better understanding of the mechanisms and pathogenesis associated with a variety of environmentally-induced or genetically-based birth defects. Our interest in modeling human genetic malformation syndromes and opportunities for collaborative efforts with molecular geneticists who have produced transgenic mice and mice with targeted gene modifications have proven productive in our attempt to better understand the developmental basis for a variety of severe malformations of the brain including anencephaly, holoprosencephaly, and hydrocephaly. Focusing on teratogens of significant human relevance, we have identified selected cell populations that are particularly vulnerable to insult at specific embryonic developmental stages. Of special interest are malformations involving the craniofacial region, including failure of the neural tube to close. Since neural crest cell populations play a key role in the genesis of many of the induced malformations, we have focused on characteristics of this cell population that impart its selective vulnerability to a variety of teratogens as well as genetically-based disturbances. Studies in progress include examination of the genesis of a wide spectrum of CNS abnormalities in an animal model for fetal alcohol syndrome. Additionally, we are utilizing an alcohol self administration mouse model to test agents, including selected antioxidants, that can ameliorate alcohol's teratogenicity. Among the methodologies currently used in this lab are whole embryo culture, confocal microscopy, in situ hybridization, microarray and proteomic analyses, and high resolution magnetic resonance imaging.

Selected Publications

  • Waage-Baudet H, Dunty WC Jr, Dehart DB, Hiller S, Sulik KK. Immunohistochemical and microarray analyses of a mouse model for the Smith-Lemli-Opitz syndrome. Dev Neurosci. 2005;27(6):378-96.
  • Sulik KK. Genesis of alcohol-induced craniofacial dysmorphism. Exp Biol Med (Maywood). 2005 Jun;230(6):366-75.
  • Chen SY, Charness ME, Wilkemeyer MF, Sulik KK. Peptide-mediated protection from ethanol-induced neural tube defects.Dev Neurosci. 2005 Jan-Feb;27(1):13-9.
  • Chen SY, Dehart DB, Sulik KK. Protection from ethanol-induced limb malformations by the superoxide dismutase/catalase mimetic, EUK-134. FASEB J. 2004 Aug;18(11):1234-6.
  • Wilkemeyer MF, Chen SY, Menkari CE, Sulik KK, Charness ME. Ethanol antagonist peptides: structural specificity without stereospecificity. J Pharmacol Exp Ther. 2004 Jun;309(3):1183-9.
  • Waage-Baudet H, Lauder JM, Dehart DB, Kluckman K, Hiller S, Tint GS, Sulik KK. Abnormal serotonergic development in a mouse model for the Smith-Lemli-Opitz syndrome: implications for autism. Int J Dev Neurosci. 2003 Dec;21(8):451-9.
  • Wilkemeyer MF, Chen SY, Menkari CE, Brenneman DE, Sulik KK, Charness ME. Differential effects of ethanol antagonism and neuroprotection in peptide fragment NAPVSIPQ prevention of ethanol-induced developmental toxicity. Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8543-8.