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The endothelial-specific deletion of CD146 in CD146EC-KO mice was further confirmed in tumor sections (Fig. S2).

For T. b. brucei, the usefulness of this triple marker to monitor the entire parasite cycle in both tsetse flies and mice was further demonstrated.

Marginal level dystrophin expression in 3cv and uko/3cv mice was further illustrated by immunofluorescence staining (Figure 2B).

The observed spontaneous liver damage in Smad7liver-KO mice was further investigated by histological and immunohistochemical analyses.

Generation of heparanase KO mice was further demonstrated by biochemical analysis revealing longer and more homogenous HS chains in Hpse-KO compared to wt mice.

The retinal origin of light aversion behaviour in TKO mice was further investigated by either eliminating BLA with bilateral axotomy or generating a response comparable to that seen in wildtype animals by specifically activating retinal neurons using Channelrhodopsin-2.

Bone resorption and formation in Tshr−/− mice were further enhanced by thyroxine replacement.

As Tek+/CreCD146floxed/floxe mice (CD146EC-KO mice) were viable, these mice were further bred to Tek+/+CD146floxed/floxed mice (WT mice), resulting in 50%% CD146EC-KO mice and 50 % WT mice, both of which were used for subsequent investigations (Fig. 1B).

Tek+/CreCD146floxed/floxed mice (CD146EC-KO mice) were viable, and these mice were further cross-bred with Tek+/+CD146floxed/floxed mice, resulting in 50%% Tek+/CreCD146floxed/floxed mice (CD146EC-KO mice) and 50%% Tek+/+CD146floxed/floxed mice (WT mice).

To further generate endothelial-specific CD146 knockout mice (CD146EC-KO mice), CD146floxed/floxed mice were further bred to Tek+/Cre mice (Strain Name: B6.Cg-Tg(Tek-cre)12Flv/J, The Jackson Laboratory), which specifically expressed Cre recombinase in ECs.

Tnf−/− mice were further backcrossed into congenic C57BL/6 background (N10).