Data Sheet 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.docx by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 7_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 3_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 2_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 4_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Data Sheet 5_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip by Haiyan Liao (6100043)

“…RNA pull-down, RNA immunoprecipitation (RIP), and actinomycin D experiments were used to show that circ_0074158 impacts endothelial barrier function in sepsis by reducing the stability of the host gene CTNNA1 (mRNA) after binding to EIF4A3.</p>Results<p>In both LPS-treated human umbilical vein endothelial cells (HUVECs) and cecal ligation and puncture (CLP) murine models, the overexpression of hsa_circ_0074158 (the mouse homolog of hsa_circ_0074158 is named circ_Ctnna1) significantly decreased CTNNA1 mRNA stability and increased endothelial hyperpermeability, while its knockdown restored barrier integrity. …”

Table 1_Puf4 -mediated oxidative stress virulence attenuation in Cryptococcus neoformans.docx by Chenhao Suo (7022351)

“…Biochemical analysis revealed that Puf4 overexpression led to significant increases in both total carbohydrate and glycogen content. …”

Data Sheet 1_Sleep is enhanced in aged male mice that overexpress calcium/calmodulin-dependent protein kinase IV.docx by Sierra P. Feeney (21466928)

“…Conversely, female mice overexpressing CaMKIV displayed no significant differences in the percentage of time spent in each vigilance state compared to their wild-type counterparts, regardless of age. …”

A) Expression of known ‘tendon’ transcription factors, B) TGFβ and C) ECM genes measured with RNA-seq. by Heather L. Dingwall (14573796)

Neonatal deletion of Yap in Scx-lineage cells disrupts collagen production in the tendon during postnatal development. by Heather L. Dingwall (14573796)

Table 4_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.xlsx by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Table 1_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.docx by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Image 2_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.tif by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Table 3_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.xlsx by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Table 2_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.docx by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Table 7_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.xlsx by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Table 6_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.xlsx by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Table 5_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.xlsx by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Image 1_Antifungal mechanism and transcriptome analysis of Bacillomycin D-C16 against Fusarium oxysporum.tif by Fuxing Lin (7418234)

“…Furthermore, nearly all DEGs related to DNA replication were significantly suppressed. Biochemical assays confirmed these observations: Reduced activities of mitochondrial enzymes [malate dehydrogenase (MDH), isocitrate dehydrogenase (IDH), pyruvate dehydrogenase (PDH), and complexes I–V], decreased mitochondrial membrane potential, and diminished ATP content collectively indicated mitochondrial dysfunction. …”

Influence of Kar4 deletion on low affinity PRE sites. by Sandrine Pinheiro (21553774)

“…The F indicates that the total fraction of expressing cells is significantly lower (t-test: p-val < 0.05) than the expression from the promoter with two consensus PRE sites. …”