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Table 2 and Figure 3 C demonstrate that the association of the DSCR9 gene on the 21q22.13 loci meets the genome-wide significance criterion of P<5×10−8 in determining eye color.

Table 2 and Figure 3 C demonstrate that the association of the LYST gene on the 1q42.3 loci meets the genome-wide significance criterion of P<5×10−8 in determining eye color.

Fig 8.

Multiplex RT-PCR results in figure 6B shows that AreA deletion mutants transcribe less methylammonium transporter genes than wild-type suggesting that areA acts as a transcriptional activator for meaA and mepA.

Figure 4C shows that mepA deletion mutants take up methylammonium at a lower rate than wildtype A. nidulans cells suggesting mepA's role as an ammonium transporter.

Figure 4C shows that meaA deletion mutants take up less methylammonium at 1mM final methylammonium concentration than wildtype A. nidulans suggesting meaA functions as an ammonium transporter.

Both RT-PCR and Western blot analyses, found in Fig. 4 A, showed that Wnt5a significantly decreased the expression level of β-catenin in melan-a cells. Co-infection analyses displayed in Fig 4 C and D each showed that Wnt5a down-regulated the expression levels of these pigmentation-related mRNAs and proteins upregulated by Wnt3a. These results, supported by the tyrosinase activity assay in Fig 4 B, suggested that Wnt5a antagonized the canonical Wnt signaling pathway in melan-a cells.

The results displayed in Fig. 3 show that Wnt5a increased the expression levels of Ror2, c-JUN, JNK1 and JNK2 in a time-dependent manner which demonstrates activation of Wnt/Ror2 signaling pathways via Wnt5a.

Wnt5a inhibited the tyrosinase activity of melan-a cells in a dose-dependent manner compared to the control as displayed in Fig. 2A. This was confirmed by the tyrosinase activity assay results in Fig. 2B, decreased protein levels of tyrosinase and TRP1 due to Wnt5a presented in Fig. 2 C and D, and also by subcutaneous implantation experiments presented in Fig. 2 E.

The results displayed in figure 1 C and D. indicate the ratio of proliferating AdWnt5a-infected cells is lower than that in control cells. This would imply that “Wnt5a inhibited the proliferation of melan-a cells.”

"These phenotypes correlate with miss-routing of the YAT plasma membrane transporters AgtA (glutamate) and PrnB (proline) to the vacuole under conditions that, in the wild type, result in their delivery to the plasma membrane. "

Plekhg4-GTPase association is demonstrated in Fig 3. B, and the GTPase activation by Plekhg4 is shown in Fig 3. A. Together these results demonstrate Plekhg4’s GEF function.

Insets of fluorescent microscopy in Fig. 4 show cytoskeletal features exhibited by Plekhg4 expression, demonstrating how it plays a role in the regulation the actin cytoskeleton

Fig. 2A,B, along with Fig. 1B show that the HINT1 KO fibroblasts demonstrate calcium ion dysregulation, While the immunoblots displayed in Fig. 3A-D, revealed that the decreased ATP-induced Ca2+ entry is likely a consequence of down-regulated expression of Orai1 and STIM1 proteins.

The results presented in Fig. 4 (A-H) suggest “that xIQGAP1 is necessary for Wnt-related early embryogenesis” and functions as an intermediate molecule in the pathway. Additionally, the results in Fig 5 also support that binding between xDVL2 and xIQGAP1 plays an important role in canonical Wnt signaling.

Figure 2 compares expression of ars operon genes in arsR deletion mutants with wild-type. Expression of ars operon genes is significantly increased in the deletion mutant proving the arsR gene acts as an ars operon repressor.

EMSA results in figure 2 prove OxyR binds to the promoter regions of several P. aerugenosa genes. Additionally, figure 3 shows that expression of dps, pvdS and trxB2 genes increased in the presence of OxyR activated by H2O2.

Figure 3D shows that repression, driven by the central region of BCL-6, was affected by MTA3 depletion. It can be concluded that MTA3 contributes to transcriptional repression by Gal4-BCL-6 through interaction with a transcriptional repression domain in the central region of BCL-6.

Figure 3 shows that TERT expression levels are decreased when PITX1 expression is high. Figure 4 further details that TERT expression is controlled through PITX1 binding to the promoter region of TERT.