Category:Team The Molecular Menace

Figure 6. When SPIN90 was knocked out, neurite outgrowth was inhibited. This was shown by comparing the length of the longest neurite and the length of shorter neurites of wild-type and of SPIN90 knocked-out hippocampal neurons.

Fig. 5 shows the aggregation of human platelets was reduced by increasing concentration of aprotinin. Curve a was the control(without the presence of aprotinin)

Figure 2. HeLa cells exhibited a higher rate of de novo pyrimidine synthesis in the presence of growth factors and amino acids. It was then concluded that mTORC1 activates de novo pyrimidine synthesis.

Figure 2. Macrophage populations were activated in CD200-/- mice. This was observed in the increase of CD11b+ population and lymph node macrophages, and the change to a thick, multi-cell layer of MOMA-1+.

Fig. 4: Aprotinin inhibits the ability of thrombin to induce a fibrin clot. The fibrinogen concentration was contant at curve a while the clotting time increased from curve b to e with the presence of aprotinin

Figure 2B. Bt-KTI inhibits the enzymatic activity of trypsin

Fig 3: Bt-KTI inhibits plasmin formation

Fig. 1D: Textilinin-1 negatively regulated blood loss in a mouse tail vein model

Figure 1 (A to H). Lack of GDE2 in spinal cords of mice leads to a loss of spinal motor neurons (MN) and V0 interneurons.

Table 1: textilinin-1 shows inhibition activity of plasmin and trypsin(low Ki values)

Fig. 5 shows SNP1 could degrade structural hydroxyproline-rich protein into small fragments.

Figure 2 The rate and incidence of telomere fusions decrease in cells in the absence of Rif1. In the presence of Rif1, nonhomologous end joining is promoted, which leads to double-stranded break repair.

Figure 1 (L to N). When GDE2 was overexpressed with Dll1 in chick spinal cords, GDE2's ability to induce neuron differentiation increased. This was shown by the increased Isl2+ motor neurons (red) in the presence of GDE2 and Dll1 compared to GDE2 by itself and Dll1 by itself.