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Faculty Barbara E. Kream
Professor, Department of Medicine and Genetics and Developmental
Biology
Director, M.D./Ph.D. Combined Degree Program
kream@nso1.uchc.edu
Areas of Interest:
The major interest of our laboratory has been to elucidate the
mechanisms by which hormones and growth factors regulate bone remodeling
in postnatal life, with an emphasis on the development and
characterization of transgenic and mutant mouse models. Our current
projects include investigating the roles of insulin-like growth factor
and glucocorticoids on bone remodeling and examining the role that a
dominant negative member of the CREM transcription factor family plays
in parathyroid hormone-dependent gene expression in osteoblasts.
Lab Rotation Projects:
The current research projects in the laboratory involve using transgenic
and knockout mouse models to understanding the role of hormones and
growth factors in bone biology. The specific areas of interest include
the role of insulin-like growth factor-I in bone development and
remodeling, molecular mechanisms by which endogenous glucocorticoids
promote bone mineralization and the role of ATF/CREB transcription
factors in osteoblast differentiation.
Selected Publications:
Lengner CJ, Steinman HA, Gagnon J, Kream BE, Stein GS, Lian JB, Jones
SN 2006 Osteoblast differentiation and skeletal development are
regulated by Mdm2-p53 signaling. J Cell Biol. 172:909-921.
He J, Rosen CJ, Adams DJ, Kream BE 2006 Postnatal growth and bone mass
in mice with IGF-I haploinsufficieny. Bone 38:826-35.
Jiang J, Lichtler AC, Gronowicz GA, Adams DJ, Clark SH, Rosen CJ, Kream
BE 2006 Transgenic mice with osteoblast-targeted insulin-like growth
facto-I show increased bone remodeling. Bone Epub, April 24.
Liu F and Kream BE Identification of novel Crem isoforms expressed by
osteoblasts 2005 Calcif Tiss Int. 77:91-95.
Liu F, Woitge HW, Braut A, Kronenberg MS, Lichtler AC, Mina M, Kream
BE 2004 Expression and activity of osteoblast-targeted Cre recombinase
transgenes in murine skeletal tissues. Int J Dev Biol 48:645-53.
Sher LB, Woitge HW, Adams DJ, Krozowski Z, Harrison JR and Kream BE
2004 Transgenic expression of 11ß-hydroxysteroid dehydrogenase type 2 in
osteoblasts reveals an anabolic role for endogenous glucocorticoids in
bone. Endocrinology 145:922-929.
Nervina JM, Tetradis S, Huang, Y, Harrison D, Molina C and Kream BE
2003 Expression of inducible cAMP early repressor is coupled to the cAMP-protein
kinase A signaling pathway in osteoblasts. Bone 32:483-490.
Harrison JR, Woitge HW and Kream BE 2002 Genetic approaches to
determine the role of glucocorticoid signaling in osteoblasts. Endocrine
17:37-42.
Woitge HW, Harrison JR, Ivkosic A, Krozowski Z and Kream BE 2001
Cloning and in vitro characterization of Col1a1-11ß-hydroxysteroid
dehydrogenase type 2 transgenes as models for osteoblast-selective
inactivation of natural glucocorticoids. Endocrinology 142:1341-1348.
Bogdanovic Z, Huang Y-F, Dodig M, Clark SH, Lichtler AC and Kream BE
2000 Parathyroid hormone inhibits collagen synthesis and the activity of
rat Col1a1 transgenes mainly by a cAMP-mediated pathway in mouse
calvariae. J Cell Biochem 77:149-158.
Woitge H and Kream BE 2000 Calvariae from fetal mice with a disrupted
Igf1 gene have reduced rates of collagen synthesis but maintain
responsiveness to glucocorticoids. J Bone Miner Res 15:1956-1964. |
