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gap decrease » gain decreased (Expand Search), step decrease (Expand Search), _ decrease (Expand Search)
a decrease » _ decrease (Expand Search), _ decreased (Expand Search), _ decreases (Expand Search)
gap decrease » gain decreased (Expand Search), step decrease (Expand Search), _ decrease (Expand Search)
a decrease » _ decrease (Expand Search), _ decreased (Expand Search), _ decreases (Expand Search)
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Data Sheet 1_Knockdown of annexin A2 enhances the host cell apoptosis induced by Eimeria tenella.zip
Published 2025“…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. …”
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Data Sheet 6_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip
Published 2025“…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. …”
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3751
Data Sheet 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.docx
Published 2025“…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. …”
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3752
Data Sheet 7_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip
Published 2025“…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. …”
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3753
Data Sheet 3_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip
Published 2025“…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. …”
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Table 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.xlsx
Published 2025“…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. …”
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Data Sheet 2_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip
Published 2025“…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. …”
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Image 1_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.tif
Published 2025“…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. …”
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Data Sheet 4_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip
Published 2025“…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. …”
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Data Sheet 5_Mechanistic study of the hsa_circ_0074158 binding EIF4A3 impairing sepsis-induced endothelial barrier.zip
Published 2025“…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. …”
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Table 2_Clinical features and genetic analysis of acrodermatitis enteropathica in an ethnic minority infant from Western China: a case report and literature review.xlsx
Published 2025“…Her serum zinc level significantly decreased (0.19 mg/L). Whole-exome sequencing revealed a homozygous c.197G > T(p. …”
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Table 1_Clinical features and genetic analysis of acrodermatitis enteropathica in an ethnic minority infant from Western China: a case report and literature review.xlsx
Published 2025“…Her serum zinc level significantly decreased (0.19 mg/L). Whole-exome sequencing revealed a homozygous c.197G > T(p. …”