Category:Team Bonfire

Figure 2: Moreover, we found a significantly increased level of Ki-67 expression on LSKs from Nrf2−/− when compared with WT bone marrow in vivo (Fig. 2c), in concordance with the enhanced proliferation observed in vitro.

Figure 4: While Alexa dye-coupled VEGF-A and VEGF-C were readily taken up by cultured mouse control endothelial cells, knockdown of Pard3 or Dab2 significantly decreased the perinuclear accumulation of VEGF-A and VEGF-C (Fig. 4a–c). Surface biotinylation experiments further confirmed that VEGF-C-induced internalization of VEGFR3 and VEGFR2 was impaired in Dab2 knockdown or Pard3 knockdown cells (Fig. 4d,e).

Figure 4: While Alexa dye-coupled VEGF-A and VEGF-C were readily taken up by cultured mouse control endothelial cells, knockdown of Pard3 or Dab2 significantly decreased the perinuclear accumulation of VEGF-A and VEGF-C (Fig. 4a–c). Surface biotinylation experiments further confirmed that VEGF-C-induced internalization of VEGFR3 and VEGFR2 was impaired in Dab2 knockdown or Pard3 knockdown cells (Fig. 4d,e).

Figure 2: Although the proportions of B cells, T cells, dendritic cells and Ly6ChighMac1+ inflammatory monocytes were not altered between wild-type and Trib1−/− splenocytes, F4/80+Mac1+ macrophages, which also expressed Mrc1 (also called MR), Arg1 and Fizz1 (also called Retnla), were markedly reduced and Siglec-F+CCR3+ eosinophils were absent in Trib1−/− spleens (Fig. 1a and Supplementary Figs 1 and 2).

Figure 2: Although the proportions of B cells, T cells, dendritic cells and Ly6ChighMac1+ inflammatory monocytes were not altered between wild-type and Trib1−/− splenocytes, F4/80+Mac1+ macrophages, which also expressed Mrc1 (also called MR), Arg1 and Fizz1 (also called Retnla), were markedly reduced and Siglec-F+CCR3+ eosinophils were absent in Trib1−/− spleens (Fig. 1a and Supplementary Figs 1 and 2).

Figure 2: Although the proportions of B cells, T cells, dendritic cells and Ly6ChighMac1+ inflammatory monocytes were not altered between wild-type and Trib1−/− splenocytes, F4/80+Mac1+ macrophages, which also expressed Mrc1 (also called MR), Arg1 and Fizz1 (also called Retnla), were markedly reduced and Siglec-F+CCR3+ eosinophils were absent in Trib1−/− spleens (Fig. 1a and Supplementary Figs 1 and 2). In contrast, the neutrophil population was increased in Trib1−/− spleens (Fig. 1a and Supplementary Fig. 3).

In figure 1 Rnf2 is shown to regulate primordial germ cell development, as seen through the effects of Rnf2 mutants

Figure 2 shows human coronavirus-Erasmus Medical Center (hCoV-EMC) tail spike binding to DPP4 which is the event needed for viral infection, Figure 3 shows DPP4 is present on hCoV-EMC succeptible cells and figure 4 confirms DDP4 is essential for the virus infection.

Figures 1 and 4 in this publication shwo that CALHM1 is involved in voltage-dependent gating and that the channel works with calcium.

Through work with CALHM1 knockout mutants,it was shown (FIG. 4) that CALHM1 is involved in the taste-evoked ATP release from taste cells.

Fig. 3; Fig 4; demonstrate that mysostatin inhibits the activation of the Akt signaling pathway in differentiating HuSkMC

Figure 1; Indicates a significant inhibition of fibroblast [NIH3T3,

mouse] cell proliferation by myostatin [recombinant, bovine] compared to control.

Myostatin fibroblast inhibition directly stated in: Results

Section/1st paragraph/last sentence.

Figure 4 shows sodium-sensitive cation currents in TMC-1 expressing cells indicating its role as a sodium channel. In supplementary figure 8 the authors also confirm TMC-1's localization to the plasma membrane using fluorescence imaging, further supporting the finding of its role as a sodium channel complex.

Figure 2 in this publication displays data that the authors found to indicate that Drd2 knockout mice were hyper-responsive with higher neuroinflammation

Responses of insulin action.. Section; Fig 3; muscle protein kinase Akt intermediate phosphorylation was measured due to is role in the insulin signaling pathway, transgenic mice showed greater levels [inhibition of myostatin] of phosphorylation

Results section/ Increased muscle weight and CK activity... Section; Fig. 7 B; Show Creatine Kinase activity increased by myostatin expression inhitbion in vivo [mice], activity bio marker used. Mice had Severe Combined Immunodeficiency and no MSTN mutations

Results section/ Myostatin reduces diameters...section/last sentence; Fig. 5c; states myostatin inhibits genes required for muscle maintenance [homeostatsis of muscle] instead of alternative atrophy pathway

Fig. 1 & 4A