The goals of my research are to understand the molecular events associated with retinoic acid-induced teratogenesis. To achieve this end, my immediate needs are to broaden my research skills, in part through interactions with other researching prominent approaches and refine the techniques I currently use, as well as to continue to grow in the ability to critically analyze research problems and concepts, and to develop innovative experimental designs. This award will significantly reduced my teaching and service responsibilities to no more than 10 to 15% of my time so that I can concentrate almost exclusively on research activity within my own laboratory, for the continuation, development, and enhancement of collaborations within Temple University and with scientists at other institutions. In addition, it will provide additional time and monies for travel to meetings, workshop and individual laboratories to enhance my research career and program. Temple University School of Medicine agrees to reduce my teaching and service responsibilities so that they will be no more than 10 to 15% of my time and to provide me with sufficient space, full use of equipment and shared resources and abilities to purchase and maintain specialized equipment to enhance my research program. Departmental budget will not be reduced because of this award assuring that at the end of this award the School of Medicine shall resume financial obligation for full payment of salary and fringe benefits at a level commensurate with meritorious continuous service to the institution. Research proposed in this application deals with the identification and characterization of the role of ANALYZE-Beta in both normal and teratogenic development. More specifically using a variety of molecular biology approaches, I will study the molecular regulation and morphological consequences of ANALYZE-beta expression during development in mouse embryos treated with normal and teratogenic doses of retinoic acid.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Modified Research Career Development Award (K04)
Project #
1K04HD001076-01
Application #
2194653
Study Section
Human Embryology and Development Subcommittee 1 (HED)
Project Start
1994-06-01
Project End
1999-05-31
Budget Start
1994-06-01
Budget End
1995-05-31
Support Year
1
Fiscal Year
1994
Total Cost
Indirect Cost
Name
Temple University
Department
Biochemistry
Type
Schools of Medicine
DUNS #
City
Philadelphia
State
PA
Country
United States
Zip Code
19122
Zhang, Z P; Gambone, C J; Gabriel, J L et al. (1998) Arg278, but not Lys229 or Lys236, plays an important role in the binding of retinoic acid by retinoic acid receptor gamma. J Biol Chem 273:34016-21
Scafonas, A; Wolfgang, C L; Gabriel, J L et al. (1997) Differential role of homologous positively charged amino acid residues for ligand binding in retinoic acid receptor alpha compared with retinoic acid receptor beta. J Biol Chem 272:11244-9
Wolfgang, C L; Zhang, Z; Gabriel, J L et al. (1997) Identification of sulfhydryl-modified cysteine residues in the ligand binding pocket of retinoic acid receptor beta. J Biol Chem 272:746-53
Korcz, A; Soprano, D R; Soprano, K J (1995) Tyrosine protein kinase expression in long-term quiescent WI-38 cells following growth factor simulation. J Cell Biochem 59:42-52
Soprano, D R; Soprano, K J (1995) Retinoids as teratogens. Annu Rev Nutr 15:111-32
Tairis, N; Gabriel, J L; Soprano, K J et al. (1995) Alteration in the retinoid specificity of retinoic acid receptor-beta by site-directed mutagenesis of Arg269 and Lys220. J Biol Chem 270:18380-7
Jiang, H; Soprano, D R; Li, S W et al. (1995) Modulation of limb bud chondrogenesis by retinoic acid and retinoic acid receptors. Int J Dev Biol 39:617-27