Figure 2 from Targeting PRMT1 Reduces Cancer Persistence and Tumor Relapse in <i>EGFR</i>- and <i>KRAS</i>-Mutant Lung Cancer by Xiaoxiao Sun (20589448)

“…<p>PRMT1 knockdown decreases persistence in STAT1-high <i>EGFR</i>^<i>mut</i> and <i>KRAS</i>^<i>G12C</i> lung cancer cell lines. …”

FGF18 injections increase chondroprogenitors and extracellular matrix and reduce chondrocyte hypertrophy after TMJ experimental degeneration. by Flavia Gomes Velasque Gama (21175112)

Data Sheet 1_Knockdown of annexin A2 enhances the host cell apoptosis induced by Eimeria tenella.zip by Jixia Wang (1685902)

“…Following ANXA2 knockdown, the cell apoptosis rate, caspase-3 activity, and Bax expression levels were significantly increased (P < 0.01), whereas the infection rate and Bcl-2 expression levels were significantly decreased (P < 0.01) compared to the group infected with E. tenella alone. …”

FGF18 injections increase cartilage thickness, chondrocyte proliferation and induce healing after TMJ experimental degeneration. by Flavia Gomes Velasque Gama (21175112)

Data Sheet 6_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 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. …”

Table 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.xlsx 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. …”

Image 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.tif 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. …”

Data Sheet 2_Identification of potential miRNA biomarkers for neurobrucellosis diagnosis.pdf by Meiling Liu (390553)

“…Additionally, RT-qPCR results revealed decreased levels of VAV3 (vav guanine nucleotide exchange factor 3, a target of miR-499a-5p) and IGF1 (insulin like growth factor 1, a target of miR-576-5p) in the CSF samples of NB patients.…”

Table 1_Identification of potential miRNA biomarkers for neurobrucellosis diagnosis.xlsx by Meiling Liu (390553)

“…Additionally, RT-qPCR results revealed decreased levels of VAV3 (vav guanine nucleotide exchange factor 3, a target of miR-499a-5p) and IGF1 (insulin like growth factor 1, a target of miR-576-5p) in the CSF samples of NB patients.…”

Table 3_Identification of potential miRNA biomarkers for neurobrucellosis diagnosis.xlsx by Meiling Liu (390553)

“…Additionally, RT-qPCR results revealed decreased levels of VAV3 (vav guanine nucleotide exchange factor 3, a target of miR-499a-5p) and IGF1 (insulin like growth factor 1, a target of miR-576-5p) in the CSF samples of NB patients.…”

Table 4_Identification of potential miRNA biomarkers for neurobrucellosis diagnosis.xlsx by Meiling Liu (390553)

“…Additionally, RT-qPCR results revealed decreased levels of VAV3 (vav guanine nucleotide exchange factor 3, a target of miR-499a-5p) and IGF1 (insulin like growth factor 1, a target of miR-576-5p) in the CSF samples of NB patients.…”

Table 2_Identification of potential miRNA biomarkers for neurobrucellosis diagnosis.xlsx by Meiling Liu (390553)

“…Additionally, RT-qPCR results revealed decreased levels of VAV3 (vav guanine nucleotide exchange factor 3, a target of miR-499a-5p) and IGF1 (insulin like growth factor 1, a target of miR-576-5p) in the CSF samples of NB patients.…”

Data Sheet 1_Identification of potential miRNA biomarkers for neurobrucellosis diagnosis.pdf by Meiling Liu (390553)

“…Additionally, RT-qPCR results revealed decreased levels of VAV3 (vav guanine nucleotide exchange factor 3, a target of miR-499a-5p) and IGF1 (insulin like growth factor 1, a target of miR-576-5p) in the CSF samples of NB patients.…”

Table 6_Identification of potential miRNA biomarkers for neurobrucellosis diagnosis.xlsx by Meiling Liu (390553)

“…Additionally, RT-qPCR results revealed decreased levels of VAV3 (vav guanine nucleotide exchange factor 3, a target of miR-499a-5p) and IGF1 (insulin like growth factor 1, a target of miR-576-5p) in the CSF samples of NB patients.…”