Pbx deficient mice
Using gene targeting techniques, we have created mice that are null for
Pbx1. Their characterization shows that Pbx1 is essential for development.
The phenotypes of Pbx1 null embryos provide compelling support for its
in vivo contributions to Hox function during many aspects of embryonic
development. These mice are being used to investigate the roles of
Pbx1 in various cellular signaling and growth control pathways.
Publications:
Selleri
L, Depew, MJ, Jacobs Y, Chanda SK, Tsang, KY, Cheah KSE, Rubenstein JLR,
O'Gorman S, Cleary ML
Requirement for Pbx1 in patterning of the skeleton and programming
chondrocyte proliferation and differentiation.
Development 128:3543-3557, 2001.
DiMartino
JF, Selleri L, Traver D, Firpo MT, Rhee J, Warnke R, O'Gorman S, Weissman
IL, Cleary ML
The Hox cofactor and proto-oncogene Pbx1 is required for maintenance
of definitive hematopoiesis in the fetal liver.
Blood 98:618-626, 2001.
Kim
SK, Selleri L, Lee JS, Zhang AY, Gu X, Jacobs Y, Cleary ML
Pbx1 inactivation disrupts pancreas development and in Ipf1-deficient
mice promotes diabetes mellitus.
Nature Genetics 30:430-435, 2002.
