In addition, C57Bl/6J mice were chosen for the Ginsenoside-F5 antibody blocking studies because the C57 strain is an established and well-characterized model of dietinduced obesity, whereas FVB mice were used in the microscopy studies because the transgenic mice with GFP expression were only available on FVB background. There are divergent reports in the literature regarding the effects of high fat diet on FVB mice �C there are reports that FVB mice are resistant to diet-induced obesity, whereas others report that this strain does develop diet-induced obesity, albeit to a lesser extent than the C57 strain. Our data in FVB mice are consistent with the results by Martin et al, i.e. the high fat diet-fed FVB mice did develop dietinduced obesity. Nevertheless, since energy metabolism is known to be very sensitive to strain background, and results obtained using one strain generally cannot be assumed to apply to other UNC669 strains without some experimental justification. Several studies in recent years have explored the feasibility of fat tissue reduction by disrupting adipose tissue vasculature. The discovery that progenitors for white fat cells are derived from the mural cell compartment of adipose tissue vasculature will undoubtedly increase interest in this approach. While reduction in body weight has been achieved in mice after anti-vascular or anti-angiogenic treatment, some caution is warranted in adapting this to clinical therapy, since the indiscriminant depletion of overall fat mass may lead to harmful lipodistrophic effects. Any future therapeutic approach that seeks to deplete fat mass must be carefully evaluated for this potential drawback. Taken together, our results indicate that angiogenesis from local preexisting vasculature �C and not the contribution of BMDCs �C primarily sustains new vessel formation in fat tissue during DIO. Antiangiogenic treatment by antibody blockade of VEGFR2 but not of VEGFR1 restricted adipose tissue expansion. These data provide novel insight for the potential targeting of the fat vasculature to control DIO. The field of protein crystallization, which previously focused almost entirely on the optimization of crystallization strategies, is now increasingly addressing the improvement of the crystallization properties of the proteins themselves. This trend began in the early 1990’s, with the advent of molecular biology techniques and mass spectrometry. The use of these techniques allowed scientists to focus crystallization efforts on the most stable domains of target proteins, as identified by their pattern of resistance to limited proteolysis. Stable domains crystallize more readily and often result in better-diffracting crystals. Success rates were further increased by expressing many variations of the protein domain, as differences of a few residues at the N- or C- termini often have dramatic effects on soluble protein expression and protein crystallization. Graslund et al. found that by screening ten derivatives of a given protein domain instead of one, the probability of generating a soluble protein increased two-fold and the probability of generating 
a structure increased four-fold. Crystallization can also be promoted by changing the surface properties of the protein to reduce the conformational entropy of surface residues. The most straight-forward approach is to use reductive methylation of surface lysine residues. In large, systematic studies, lysine methylation rescued 6% of a set of recalcitrant proteins. Surface entropy can also be reduced by site-directed mutagenesis of clusters of charged residues.