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defect ( Bleich et al . 1999 ). The difficulty of maintaining these mice and their complicated systemic defects made them unsuitable for studies on the role of the MR in other tissue compartments or cell types. Development of the Cre recombinase-LoxP

and females (except on proestrus) is unlikely to derive from preservation of some PR function (i.e., incomplete recombination by Cre). Indeed, global Pgr -knockout mice similarly show normal LH and FSH production under most conditions ( Chappell et

useful to generate tissue- (i.e. conditional knockout) or time-specific (i.e. inducible knockout) models. This is achieved by refining the gene trap and ‘conventional’ knockout strategies by the addition of LoxP or flippase (FLP) recombinase target (FRT

. Synapsin 1 promoter-controlled cre expression significantly increases adiposity of tr/tr mice The gene trap vector in tr/tr mice contains two loxP sites, flanking the splicing acceptor (SA) sequences that disrupt normal Mex3c splicing ( Fig. 5 A). In

16 activity than the previous cell-specific mouse models that we have used for detailed mechanistic studies of the effect of WNT16 on cortical bone. In these previous studies, we used Runx2-Cre and Dmp1-Cre mouse models to demonstrate that

obtained from Rodger McEver (Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Betz et al . 1998 ). Mice hemizygous for the Cre transgene were crossed with the gp130 flox mouse in which the transmembrane domain (exon 15) was flanked by loxP

been shown in these cells. Table 1 Summarizes all the different knockouts and promoter Cre lines utilized to delete Pten and its downstream targets in different skeletal lineages along with some of the key observations Conditional knockouts of Pten

the phenotype obtained in the knockout mouse model and the understanding of the physiological relevance of the gene studied. Therefore, it should be necessary to assess the tissue-specific effects of PPARs with several Cre-LoxP-based methods (i

Cre-mediated recombination to activate repressed promoters in a cell-specific manner. Examples of each of these strategies are described below as pre-clinical models of pituitary tumor gene therapy. In addition to selective expression in the pituitary

if for some of these factors produced by, and acting on, testicular cells, knockout models or spontaneous genetic defects have allowed us to understand their role on the early steps of spermatogenesis (e.g. stem cell factor (SCF), Besmer et al