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|Status||Page||User||Date/Time||GO Term (Aspect)||Reference||Evidence||Notes||Links|
|PSEAI:P95429||Vandecap, MichSt14A 23||2014-04-06 15:38:51 CDT||GO:0045892 negative regulation of transcription, DNA-templated (P)||PMID:23279839||ECO:0000314 direct assay evidence used in manual assertion|
Figure 1 A & B shows the diminished transcript levels in the presence of ExsD compared to ExsA, additionally it shows the decline of transcript levels in the presence of increased concentrations of ExsD.
|XANCP:Q8PB94||Vandecap, MichSt14A 23||2014-04-06 12:29:48 CDT||GO:0009306 protein secretion (P)||PMID:23777429||ECO:0000314 direct assay evidence used in manual assertion|
Figure 5 demonstrates the analysis of amino acid residues of the FHIPEP motif to protein–protein interactions. When HrcVR138A-c-Myc and HrcV
D161A-c-Myc were incubated with GST or GST fusion proteins, both coeluted with GST-HpaC, GST-HrpE, and GST fusions of T3S effectors but were not detected in the eluates of GST-HrcV324-645, GST-HrcN, GST-HrcU255-357, GST- HpaB, and GST-HrpB2. The absence of detectable interactions of HrcVR138A-c-Myc and HrcVD161A-c-Myc with HpaB, HrpB2, and T3S system components explains the loss-of-function phenotypes and implies that these interactions are needed for protein function.
|HUMAN:FAF1||Vandecap, MichSt14A 23||2014-04-03 13:26:55 CDT||GO:0008219 cell death (P)||PMID:22876279||ECO:0000315 mutant phenotype evidence used in manual assertion|
Figure 4 B & C shows the pro-apoptosis abilities of hFAF1. The plates show that in those cells where hFAF1 was knocked out there was a significant increase in cell growth, in contrast those plates where the hFAF1 was left functioning properly there was a lack of cell growth, which was due to hFAF1 ability to break down HSP 70. This is again shown in the table, which specifically points out the amount of colonies.
|YERE1:E7BAY2||Vandecap, MichSt14A 23||2014-04-03 11:25:46 CDT||GO:0004725 protein tyrosine phosphatase activity (F)||PMID:24658611||ECO:0000314 direct assay evidence used in manual assertion|
Figure 5 demonstrates LcrQ ability to negatively regulate gene expression because the graph shows limited B-galactosidase activity for LcrQ, while there is an up regulation of B-glactosidase activity for the LcrF gene that is responsible for positive gene expression.
|PSEAE:EXSA||Vandecap, MichSt14A 23||2014-04-03 11:21:23 CDT||GO:2000144 positive regulation of DNA-templated transcription, initiation (P)||PMID:24142246||ECO:0000314 direct assay evidence used in manual assertion|
Figure 8 shows that the binding site is required for transcription activation, but the paper already established activation via IDA in Fig 7
|YERE1:E7BAZ6||Vandecap, MichSt14A 23||2014-04-03 11:19:50 CDT||GO:2000144 positive regulation of DNA-templated transcription, initiation (P)||PMID:24142246||ECO:0000314 direct assay evidence used in manual assertion|
|HUMAN:FAF1||Vandecap, MichSt14A 23||2014-04-03 10:29:30 CDT||GO:0010942 positive regulation of cell death (P)||PMID:15596450||ECO:0000314 direct assay evidence used in manual assertion|
Figure 9 demonstrates hFAF1 ability to induce apoptosis, specifically through heat shock. The graph in figure 9 shows that HSP+ hFAF1 had the lowest cell viability of all samples proposed and cell viability was confirmed through 3-2, 5-diphenyltetrazolium bromide assay.
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Pages in category "MichSt14A 23"
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