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human dlat shrna silencing aav  (Vector Biolabs)


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    Vector Biolabs human dlat shrna silencing aav
    Human Dlat Shrna Silencing Aav, supplied by Vector Biolabs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    A workflow of this study (A) Overview of the mechanism of action of N-acetylgalactosamine-small interfering RNA (GalNAc-siRNA) and the seven approved GalNAc-SiRNA drugs collected in this study. (B) Schematic structure of the developed computational model for a GalNAc-siRNA. (C) Schematic workflow of the model informed GalNAc-siRNA development powered by the established computational platform.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: A computational model-powered platform to inform the development of GalNAc-conjugated siRNA therapeutics

    doi: 10.1016/j.omtn.2026.102936

    Figure Lengend Snippet: A workflow of this study (A) Overview of the mechanism of action of N-acetylgalactosamine-small interfering RNA (GalNAc-siRNA) and the seven approved GalNAc-SiRNA drugs collected in this study. (B) Schematic structure of the developed computational model for a GalNAc-siRNA. (C) Schematic workflow of the model informed GalNAc-siRNA development powered by the established computational platform.

    Article Snippet: Finally, the platform was utilized to support the development of an investigational new angiotensinogen ( AGT )-silencing GalNAc-siRNA, termed SAL0132 (developed by Shenzhen Salubris Pharmaceuticals Co., Ltd), from preclinic rats and monkey to clinical studies.

    Techniques: Small Interfering RNA

    Lnc_011797 regulates WNK1 expression in HUVECs. (A) RT-PCR analysis of lnc_011797 expression in HUVECs. (B) WNK1 mRNA expression after transfection with specific lentiviruses was analyzed via RT-PCR. The data were normalized to the control group. (C) Western blot analysis was used to assess WNK1 expression after transfection with specific lentiviruses. Data are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by the least significant difference post hoc tests). HUVECs: Human umbilical vein endothelial cells; RT-PCR: real-time polymerase chain reaction; WNK1: with-no-lysine (K) 1.

    Journal: Neural Regeneration Research

    Article Title: Lnc_011797 promotes ferroptosis and aggravates white matter lesions

    doi: 10.4103/NRR.NRR-D-24-00676

    Figure Lengend Snippet: Lnc_011797 regulates WNK1 expression in HUVECs. (A) RT-PCR analysis of lnc_011797 expression in HUVECs. (B) WNK1 mRNA expression after transfection with specific lentiviruses was analyzed via RT-PCR. The data were normalized to the control group. (C) Western blot analysis was used to assess WNK1 expression after transfection with specific lentiviruses. Data are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by the least significant difference post hoc tests). HUVECs: Human umbilical vein endothelial cells; RT-PCR: real-time polymerase chain reaction; WNK1: with-no-lysine (K) 1.

    Article Snippet: Lnc_011797-overexpressing lentivirus (oe-lnc) and silencing lentivirus (si-lnc) were constructed by Genechem Co. Ltd. (Shanghai, China).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Transfection, Control, Western Blot, Real-time Polymerase Chain Reaction

    Lnc_011797 can bind to miR-193b-3p to regulate WNK1 expression. (A) Predicted binding sites between miR-193b-3p and lnc_011797 or WNK1. Lnc_011797 contains two predicted miR-193b-3p binding sites (shown in red). (B) RT-PCR analysis of miR-193b-3p expression in HUVECs transfected with the miR-193b-3p mimic, mimic control, miR-193b-3p inhibitor, or inhibitor control. (C, D) miR-193b-3p binding to lnc_011797 (C) and WNK1 (D) was confirmed by dual luciferase reporter gene assay. (E) Lnc_011797 regulates miR-193b-3p expression. (F-I) RT-PCR (F, G) and western blotting (H, I) were used to measure WNK1 expression in cells transfected with the lnc_011797–specific lentivirus and the miR-193b-3p mimic or inhibitor. The data were normalized to the control group. Data are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by the least significant difference post hoc tests). HUVECs: Human umbilical vein endothelial cells; RT-PCR: real-time polymerase chain reaction; WNK1: with-no-lysine (K) 1.

    Journal: Neural Regeneration Research

    Article Title: Lnc_011797 promotes ferroptosis and aggravates white matter lesions

    doi: 10.4103/NRR.NRR-D-24-00676

    Figure Lengend Snippet: Lnc_011797 can bind to miR-193b-3p to regulate WNK1 expression. (A) Predicted binding sites between miR-193b-3p and lnc_011797 or WNK1. Lnc_011797 contains two predicted miR-193b-3p binding sites (shown in red). (B) RT-PCR analysis of miR-193b-3p expression in HUVECs transfected with the miR-193b-3p mimic, mimic control, miR-193b-3p inhibitor, or inhibitor control. (C, D) miR-193b-3p binding to lnc_011797 (C) and WNK1 (D) was confirmed by dual luciferase reporter gene assay. (E) Lnc_011797 regulates miR-193b-3p expression. (F-I) RT-PCR (F, G) and western blotting (H, I) were used to measure WNK1 expression in cells transfected with the lnc_011797–specific lentivirus and the miR-193b-3p mimic or inhibitor. The data were normalized to the control group. Data are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001 (one-way analysis of variance followed by the least significant difference post hoc tests). HUVECs: Human umbilical vein endothelial cells; RT-PCR: real-time polymerase chain reaction; WNK1: with-no-lysine (K) 1.

    Article Snippet: Lnc_011797-overexpressing lentivirus (oe-lnc) and silencing lentivirus (si-lnc) were constructed by Genechem Co. Ltd. (Shanghai, China).

    Techniques: Expressing, Binding Assay, Reverse Transcription Polymerase Chain Reaction, Transfection, Control, Luciferase, Reporter Gene Assay, Western Blot, Real-time Polymerase Chain Reaction

    Galectin-9 and Tim-3 expression assessed by cytometry across glioma subtypes. (A, B) Color-coded scatter bar plots represent the relative proportions of Galectin-9 + in A, Tim-3 + in B cells of indicated myeloid and lymphoid cell types across IDH classified primary and recurrent gliomas: NGB ( n = 3), IMP ( n = 14), IMR ( n = 9), IWP ( n = 13), IWR ( n = 12). Statistical differences were determined using Kruskal–Wallis test followed by Dunn’s post-hoc test for multiple comparisons at indicated p values, between NGB versus glioma subtypes, IMP versus IMR, IWP versus IWR, and IMP versus IWP. n.s. = statistically not significant. See also .

    Journal: Frontiers in Immunology

    Article Title: Interrogation of glioma immune microenvironment identifies a non-canonical role for microglial Galectin-9 in tumor cell adhesion and phagocytosis

    doi: 10.3389/fimmu.2026.1733688

    Figure Lengend Snippet: Galectin-9 and Tim-3 expression assessed by cytometry across glioma subtypes. (A, B) Color-coded scatter bar plots represent the relative proportions of Galectin-9 + in A, Tim-3 + in B cells of indicated myeloid and lymphoid cell types across IDH classified primary and recurrent gliomas: NGB ( n = 3), IMP ( n = 14), IMR ( n = 9), IWP ( n = 13), IWR ( n = 12). Statistical differences were determined using Kruskal–Wallis test followed by Dunn’s post-hoc test for multiple comparisons at indicated p values, between NGB versus glioma subtypes, IMP versus IMR, IWP versus IWR, and IMP versus IWP. n.s. = statistically not significant. See also .

    Article Snippet: Next, we tested the effect of Galectin-9 silencing on pMG behavior.

    Techniques: Expressing, Cytometry

    Galectin-9 expression in tumor and associated leukocytes in glioma. (A) Western blot showing expression of Galectin-9 in flow-sorted CD45 - (tumor), associated leukocytes (CD45 + ), GSC-23, and GSC-28. (B) Representative microscopic image of multiplex IHC stained FFPE tissue sections of primary IDH-mut (top) and IDH-wt (bottom) glioma patients ( n = 5/group). Unmixed images showing expression of Galectin-9 (green), Iba-1 (red), and DAPI (4”,6-diamidino-2-phenylindole) and composite image showing co-expression of Galectin-9 + Iba-1 + MG (crimson, highlighted by arrows) at 40× magnification. Scale bars = 50 μm. (C) Representative microscopic image of multiplex IHC stained FFPE tissue sections of primary IDH-mut (top) and IDH-wt (bottom) glioma patients ( n = 5 per group). Unmixed and composite images showing expression of Galectin-9 (green), Nestin (red), and DAPI (4”,6-diamidino-2-phenylindole) at 40X magnification. Nestin expressing glioma cells do not express Galectin-9 as shown by red and green arrows. Scale bars = 50 μm.

    Journal: Frontiers in Immunology

    Article Title: Interrogation of glioma immune microenvironment identifies a non-canonical role for microglial Galectin-9 in tumor cell adhesion and phagocytosis

    doi: 10.3389/fimmu.2026.1733688

    Figure Lengend Snippet: Galectin-9 expression in tumor and associated leukocytes in glioma. (A) Western blot showing expression of Galectin-9 in flow-sorted CD45 - (tumor), associated leukocytes (CD45 + ), GSC-23, and GSC-28. (B) Representative microscopic image of multiplex IHC stained FFPE tissue sections of primary IDH-mut (top) and IDH-wt (bottom) glioma patients ( n = 5/group). Unmixed images showing expression of Galectin-9 (green), Iba-1 (red), and DAPI (4”,6-diamidino-2-phenylindole) and composite image showing co-expression of Galectin-9 + Iba-1 + MG (crimson, highlighted by arrows) at 40× magnification. Scale bars = 50 μm. (C) Representative microscopic image of multiplex IHC stained FFPE tissue sections of primary IDH-mut (top) and IDH-wt (bottom) glioma patients ( n = 5 per group). Unmixed and composite images showing expression of Galectin-9 (green), Nestin (red), and DAPI (4”,6-diamidino-2-phenylindole) at 40X magnification. Nestin expressing glioma cells do not express Galectin-9 as shown by red and green arrows. Scale bars = 50 μm.

    Article Snippet: Next, we tested the effect of Galectin-9 silencing on pMG behavior.

    Techniques: Expressing, Western Blot, Multiplex Assay, Staining

    Gene enrichment analysis of Galectin-9 + and Galectin-9 - subpopulations of GAMs. (A) UMAP visualization of MG (left), MAC/MDM = MACs (right) based on differential expression of Galectin-9 gene in IDH-wt glioma patients ( n = 8). Cells are color coded for Galectin-9 expression. (B) Enhanced volcano plot of the variable genes in ( n = 9,372) (top) and Galectin-9 + MACs (bottom) compared to Galectin-9 - counterparts. Gray dots represent genes qualifying average log2FC cutoff of 0.5 and adjusted p -value cutoff of 0.05. The top significant genes for Galectin-9 + GAMs indicated in red. (C) Bubble plot representing the union set of phagocytic markers differentially enriched in Galectin-9 + and Galectin-9 - subpopulations of MG and MACs as indicated. The genes are annotated for their molecular function. The scaled gene expression is shown by the color-bar and the percentage expression by cells is represented by dot size.

    Journal: Frontiers in Immunology

    Article Title: Interrogation of glioma immune microenvironment identifies a non-canonical role for microglial Galectin-9 in tumor cell adhesion and phagocytosis

    doi: 10.3389/fimmu.2026.1733688

    Figure Lengend Snippet: Gene enrichment analysis of Galectin-9 + and Galectin-9 - subpopulations of GAMs. (A) UMAP visualization of MG (left), MAC/MDM = MACs (right) based on differential expression of Galectin-9 gene in IDH-wt glioma patients ( n = 8). Cells are color coded for Galectin-9 expression. (B) Enhanced volcano plot of the variable genes in ( n = 9,372) (top) and Galectin-9 + MACs (bottom) compared to Galectin-9 - counterparts. Gray dots represent genes qualifying average log2FC cutoff of 0.5 and adjusted p -value cutoff of 0.05. The top significant genes for Galectin-9 + GAMs indicated in red. (C) Bubble plot representing the union set of phagocytic markers differentially enriched in Galectin-9 + and Galectin-9 - subpopulations of MG and MACs as indicated. The genes are annotated for their molecular function. The scaled gene expression is shown by the color-bar and the percentage expression by cells is represented by dot size.

    Article Snippet: Next, we tested the effect of Galectin-9 silencing on pMG behavior.

    Techniques: Quantitative Proteomics, Expressing, Gene Expression

    Glioma cell adhesion was reduced upon Galectin-9 downregulation. (A) Representative microscopic immunofluorescence image showing staining of Galectin-9 (green), Iba-1 (red) and DAPI and their composite expression in merged image of untreated pMG controls (top), Galectin-9 siRNA treated pMG (middle) and siRNA controls (bottom). Scale bars = 90 μm. (B) Diagram showing Ibidi experimental design for pMG/GSC8-11ZsG co-culture assays for adhesion and phagocytosis. (C) Representative microscopic immunofluorescence image showing phase contrast visualization of adhered pMG and GSC8-11ZsG (green) calculated as adhesion ratio when cocultured with untreated pMG controls (top), Galectin-9 siRNA–treated pMG (middle), and siRNA controls (bottom) with GSC8-11ZsG at 2h post-incubation. Scale bars = 40 μm. (D) Scatter dot plots showing corresponding proportions as mean ± SD of % GSC8-11ZsG adhered to indicated pMG from three different fetal donors (pMG-2103, pMG-707, and pMG-1805). Error bars indicate the SD of mean. Statistical differences were determined using Kruskal–Wallis test followed by Dunn’s post-hoc test for multiple comparisons between siRNA treated versus control groups at * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. See also and .

    Journal: Frontiers in Immunology

    Article Title: Interrogation of glioma immune microenvironment identifies a non-canonical role for microglial Galectin-9 in tumor cell adhesion and phagocytosis

    doi: 10.3389/fimmu.2026.1733688

    Figure Lengend Snippet: Glioma cell adhesion was reduced upon Galectin-9 downregulation. (A) Representative microscopic immunofluorescence image showing staining of Galectin-9 (green), Iba-1 (red) and DAPI and their composite expression in merged image of untreated pMG controls (top), Galectin-9 siRNA treated pMG (middle) and siRNA controls (bottom). Scale bars = 90 μm. (B) Diagram showing Ibidi experimental design for pMG/GSC8-11ZsG co-culture assays for adhesion and phagocytosis. (C) Representative microscopic immunofluorescence image showing phase contrast visualization of adhered pMG and GSC8-11ZsG (green) calculated as adhesion ratio when cocultured with untreated pMG controls (top), Galectin-9 siRNA–treated pMG (middle), and siRNA controls (bottom) with GSC8-11ZsG at 2h post-incubation. Scale bars = 40 μm. (D) Scatter dot plots showing corresponding proportions as mean ± SD of % GSC8-11ZsG adhered to indicated pMG from three different fetal donors (pMG-2103, pMG-707, and pMG-1805). Error bars indicate the SD of mean. Statistical differences were determined using Kruskal–Wallis test followed by Dunn’s post-hoc test for multiple comparisons between siRNA treated versus control groups at * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. See also and .

    Article Snippet: Next, we tested the effect of Galectin-9 silencing on pMG behavior.

    Techniques: Immunofluorescence, Staining, Expressing, Co-Culture Assay, Incubation, Control

    Impaired phagocytic uptake of glioma cell by pMG upon Galectin-9 downregulation. (A) Representative microscopic immunofluorescence image showing phase contrast visualization of pMG, GSC8-11ZsG (green) and pMG/GSC8-11ZsG (merged) exhibiting phagocytosis when cocultured with untreated pMG controls (top), Galectin-9 siRNA–treated pMG (middle) and siRNA controls (bottom) with GSC8-11ZsG at 2h post-incubation. Scale bars = 60 μm. White boxes shows magnified image that depicts amount of GSC8-11ZsG by pMG. (B) Scatter dot plots showing mean proportions ± SD of pMG (pMG-2103, pMG-707, and pMG-1805) that phagocytosed GSC8-11ZsG (phagocytosis ratio) in untreated control, treated Galectin-9 siRNA, and siRNA control experimental conditions when co-cultured with GSC8-11ZsG. Error bars indicate the SD of mean. Statistical differences were determined using Kruskal–Wallis test followed by Dunn’s post-hoc test for multiple comparisons between siRNA-treated versus control groups at ** p < 0.01, **** p < 0.0001. (C) , Scatter dot plots showing mean proportions ± SD of pMG (pMG-2103, pMG-707, and pMG-1805) that phagocytosed GSC8-11ZsG (phagocytosis ratio) in untreated control, treated Galectin-9 neutralization Ab (MAb-13), and IgG control experimental conditions when co-cultured with GSC8-11ZsG. Error bars indicate the SD of mean. Statistical differences were determined using Kruskal–Wallis test followed by Dunn’s post-hoc test for multiple comparisons between siRNA-treated versus control groups at *** p < 0.001, **** p < 0.0001. See also .

    Journal: Frontiers in Immunology

    Article Title: Interrogation of glioma immune microenvironment identifies a non-canonical role for microglial Galectin-9 in tumor cell adhesion and phagocytosis

    doi: 10.3389/fimmu.2026.1733688

    Figure Lengend Snippet: Impaired phagocytic uptake of glioma cell by pMG upon Galectin-9 downregulation. (A) Representative microscopic immunofluorescence image showing phase contrast visualization of pMG, GSC8-11ZsG (green) and pMG/GSC8-11ZsG (merged) exhibiting phagocytosis when cocultured with untreated pMG controls (top), Galectin-9 siRNA–treated pMG (middle) and siRNA controls (bottom) with GSC8-11ZsG at 2h post-incubation. Scale bars = 60 μm. White boxes shows magnified image that depicts amount of GSC8-11ZsG by pMG. (B) Scatter dot plots showing mean proportions ± SD of pMG (pMG-2103, pMG-707, and pMG-1805) that phagocytosed GSC8-11ZsG (phagocytosis ratio) in untreated control, treated Galectin-9 siRNA, and siRNA control experimental conditions when co-cultured with GSC8-11ZsG. Error bars indicate the SD of mean. Statistical differences were determined using Kruskal–Wallis test followed by Dunn’s post-hoc test for multiple comparisons between siRNA-treated versus control groups at ** p < 0.01, **** p < 0.0001. (C) , Scatter dot plots showing mean proportions ± SD of pMG (pMG-2103, pMG-707, and pMG-1805) that phagocytosed GSC8-11ZsG (phagocytosis ratio) in untreated control, treated Galectin-9 neutralization Ab (MAb-13), and IgG control experimental conditions when co-cultured with GSC8-11ZsG. Error bars indicate the SD of mean. Statistical differences were determined using Kruskal–Wallis test followed by Dunn’s post-hoc test for multiple comparisons between siRNA-treated versus control groups at *** p < 0.001, **** p < 0.0001. See also .

    Article Snippet: Next, we tested the effect of Galectin-9 silencing on pMG behavior.

    Techniques: Immunofluorescence, Incubation, Control, Cell Culture, Neutralization