skip to content »

Molecular and Human Genetics

Houston, Texas

Department of Molecular and Human Genetics
Department of Molecular and Human Genetics
not shown on screen

William J. Craigen, M.D., Ph.D.

William J. Craigen, M.D., Ph.D.

Associate Professor, Department of Molecular and Human Genetics

Other Positions

Associate Professor, Department of Pediatrics; Program in Translational Biology and Molecular Medicine
Director, Metabolic Clinic
Medical Director, Mitochondrial Laboratory

Education

B.S., B.A., University of Texas, Austin, 1981
M.D., Ph.D., Baylor College of Medicine, 1988
Fellow, Medical Genetics, Baylor College of Medicine, 1990
Resident, Pediatrics, Baylor College of Medicine, 1992

Board Certifications

American Board of Pediatrics
American Board of Medical Genetics: Biochemical Genetics and Clinical Genetics

Professional Organizations

Member, American Society of Human Genetics
Member, Society for the Study of Inborn Errors of Metabolism
Member, American Society for the Advancement of Science
Member, The Biophysical Society Society for Inherited Metabolic Disorders

Clinical Interests

Genetic Disorders and Metabolic Disorders

Research Interests

Mitochondrial function: Mitochondria are now recognized to play a variety of important physiologic roles in various processes beyond ATP synthesis, including programmed cell death (apoptosis), retrograde signaling, cellular proliferation, and the regulation of intermediary metabolism. One area of interest in the lab is in understanding the role of the mitochondrial outer membrane permeability in the regulation of cellular energy economy, apoptosis and mammalian organ function. Voltage-dependent Anion Channels (VDAC1-3: also known as mitochondrial porins) are a family of mitochondrial outer membrane proteins that conduct small molecules across the outer membrane. VDACs also bind cytosolic kinases such as hexokinase isoforms, and may act to tether other multi-protein complexes to mitochondria. One isoform (VDAC2) functions in suppressing apoptosis by binding the multi-domain pro-apoptotic protein BAK, while other isoforms play roles in glucose metabolism, learning and memory, and fertility. Using model organisms we are interested in determining the specific functions of each isoform in biology and relating VDAC function to disease states. These studies involve biochemical, physiologic, and genetic experimentation.

Human metabolic disorders: Despite advances in identifying human metabolic diseases, pathophysiologic mechanisms are poorly understood and specific treatment strategies lacking. Others projects in the laboratory involve studies of metabolic pathways leading to human inherited disorders. Using mutant mice, our current studies are designed to understand the metabolic disturbances that are associated defects in phospholipid and fatty acid metabolism, purine and creatine synthesis, and mitochondrial respiratory chain activities. We are interested in defining cell type-specific functions for the enzymes of intermediary metabolism using knockout mice in conjunction with tissue-specific transgene expression.

Selected Publications

VDAC3 Deficient Mouse Sperm

VDAC3 Deficient Mouse Sperm.

  1. Baines CP, Kaiser RA, Sheiko T, Craigen WJ, Molkentin JD (2007). Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death. Nat. Cell Biol. 9(5): 550-5. [Pub Med]
  2. Anflous-Pharayra K, Cai ZJ, Craigen WJ (2007). VDAC1 serves as a mitochondrial binding site for hexokinase in oxidative muscles. Biochim. Biophys. Acta. 1767(2): 136-42. [Pub Med]
  3. Sabirov RZ, Sheiko T, Liu H, Deng D, Okada Y, Craigen WJ (2006). Genetic demonstration that the plasma membrane maxianion channel and voltage-dependent anion channels are unrelated proteins. J. Biol. Chem. 281(4): 1897-904. [Pub Med]
  4. Graham BH, Craigen WJ (2005). Mitochondrial voltage-dependent anion channel gene family in Drosophila melanogaster: Complex patterns of evolution, genomic organization, and developmental expression. Mol. Genet. Metab. 85(4): 308-17. [Pub Med]
  5. Cheng EH, Sheiko TV, Fisher JK, Craigen WJ, Korsmeyer SJ (2003). VDAC2 inhibits BAK activation and mitochondrial apoptosis. Science 301(5632): 513-7. [Pub Med]
  6. Sutton VR, Pan Y, Davis EC, Craigen WJ (2003). A mouse model of argininosuccinic aciduria: Biochemical characterization. Mol. Genet. Metab. 78(1): 11-6. [Pub Med]
  7. Weeber EJ, Levy M, Sampson MJ, Anflous K, Armstrong D, Brown SE, Sweatt JD, Craigen WJ (2002). The role of mitochondrial porins and the permeability transition pore in learning and synaptic plasticity. J. Biol. Chem. 277(21): 18891-7. [Pub Med]
  8. Sampson MJ, Decker WK, Beaudet AL, Ruitenbeek W, Armstrong D, Hicks MJ, Craigen WJ (2001). Immotile sperm and infertility in mice lacking mitochondrial voltage-dependent anion channel type 3. J. Biol. Chem. 276(42): 39206-12. [Pub Med]
  9. Anflous K, Armstrong D, Craigen WJ (2001). Altered mitochondrial sensitivity for ADP and maintenance of creatine stimulated respiration in oxidative striated muscles from VDAC1 deficient mice. J. Biol. Chem. 276(3): 1954-60. [Pub Med]

More Publications (PubMed)

Contact Information

William J. Craigen, M.D., Ph.D.
Department of Molecular and Human Genetics
Baylor College of Medicine
One Baylor Plaza, MS BCM225
Houston, TX, 77030, U.S.A.

Phone: 713-798-8305
Fax: 713-798-7773
E-mail:

E-mail this page to a friend