Category:Team GreyJoy

It is shown in figure 3 that ACS is strongly fluorescently labelled after exposure to MsPat with a fluorescent chloracetyl group bound to it, indicating that ACS deacetylated the protein.

As shown in figure 5, Acetyl CoA synthetase with a fluorescently marked chloracetyl group was lowered in fluorescent intensity when Rv1151c was added, indicating that Rv1151c deacetylated the protein.

It is shown in Figure 1B that the protein acetyltransferase binds an acetyl group, and in Figure 3B that the acetyl group is transfered to Acetyl CoA Synthetase.

As shown in figures 1 and 2, inactivation of Smad4 leads to a lack of development in the skeletal portion of embryonic digits.

As shown in figure 1, a mutant of uridine phosphorylase in the liver with markedly higher enzymatic content led to a significant increase in beta alanine content in the liver compared to the wild type.

As shown in figure 2, the level of NADPH in the cell is comparatively greater in cells with wild type Malic Enzyme 2 than with Malic Enzyme 2 mutants that had no enzymatic activity.

In figure 2, it is shown that relative to Malic Enzyme mutants that show no enzymatic activity, wild type Malic Enzyme leads to greater production of NADPH in a cell.

Fig 1C.

Fig 1C.

As show in Figure 1, a deletion mutation of the gene encoding EzrA leads to improper partitioning of a cell into its daughter cells

As shown in figure 1, cells with a deletion mutation in the gene for ypbR developed double septa during cytokinesis.

As indicated in figure 5, ATP is hydrolyzed at a significantly greater rate when FtsK is introduced.

As shown in figure 5, cells with a deletion mutation of varying parts of FtsK form elongate rods, which is indicative of the cell's inability to divide.

As evidenced in figure 4 by the in situ hybridization, BMP-2 RNA transcripts are present in the terminal ends of the digits as they develop from the forelimb.

It is shown by figure 3 through a direct assay that Smad4 binds to a promoter for Dlx-3, which is known to regulate patterning in the embyronic ectoderm.

It is shown by figure 3 through a direct assay that Smad4 binds to a promoter for the homeodomain Dlx-3 that is responsive to signaling by BMP-2.

It is shown by figure 3 through a direct assay that Smad1 binds to a promoter on the homeodomain Dlx-3 which regulates patterning in the embryonic ectoderm

It is shown by figure 3 through a direct assay that Smad1 binds to an area of the Dlx-3 homeodomain that is responsive to BMP-2 signaling.

It is shown by figure 6 through a direct assay that BMP induces the Dlx-3 homeodomain, which regulates patterning in the embryonic ectoderm.

It is shown by figure 1 through a direct assay that BMP-2 is involved in the induction of Dlx-3 transcription.

It is shown in figure 3 that a knockout mutation in MerTK leads to increased apoptosis rates in response to chemotherapeutic agents.

It is shown in figure 3 that a knockout mutation in MerTK leads to increased apoptosis rates in response to chemotherapeutic agents.