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anti kiaa1199  (Bioss)


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    Bioss anti kiaa1199
    (A) The iTRAQ quantitative proteomic analysis of infected CEF at 72hpi. There were 33 differentially expressed proteins between co-infection and single infection. (B) ALV-J and REV synergistically enhanced the <t>KIAA1199</t> RNA level in infected DF-1 cells at 72hpi. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates. (C) ALV-J synergized with REV to enhance the KIAA1199 protein level in DF-1 cells at 72hpi detected by western blot with anti-KIAA1199 antibody. (D) MiR-147 was the only downregulated miRNA in co-infection group. (E) ALV-J synergized with REV to inhibit the miR-147 RNA level in DF-1 cells at 72hpi. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates.
    Anti Kiaa1199, supplied by Bioss, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti kiaa1199/product/Bioss
    Average 90 stars, based on 1 article reviews
    anti kiaa1199 - by Bioz Stars, 2026-02
    90/100 stars

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    1) Product Images from "ALV-J and REV synergistically activate a new oncogene of KIAA1199 via NF-κB and EGFR signaling regulated by miR-147"

    Article Title: ALV-J and REV synergistically activate a new oncogene of KIAA1199 via NF-κB and EGFR signaling regulated by miR-147

    Journal: bioRxiv

    doi: 10.1101/338244

    (A) The iTRAQ quantitative proteomic analysis of infected CEF at 72hpi. There were 33 differentially expressed proteins between co-infection and single infection. (B) ALV-J and REV synergistically enhanced the KIAA1199 RNA level in infected DF-1 cells at 72hpi. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates. (C) ALV-J synergized with REV to enhance the KIAA1199 protein level in DF-1 cells at 72hpi detected by western blot with anti-KIAA1199 antibody. (D) MiR-147 was the only downregulated miRNA in co-infection group. (E) ALV-J synergized with REV to inhibit the miR-147 RNA level in DF-1 cells at 72hpi. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates.
    Figure Legend Snippet: (A) The iTRAQ quantitative proteomic analysis of infected CEF at 72hpi. There were 33 differentially expressed proteins between co-infection and single infection. (B) ALV-J and REV synergistically enhanced the KIAA1199 RNA level in infected DF-1 cells at 72hpi. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates. (C) ALV-J synergized with REV to enhance the KIAA1199 protein level in DF-1 cells at 72hpi detected by western blot with anti-KIAA1199 antibody. (D) MiR-147 was the only downregulated miRNA in co-infection group. (E) ALV-J synergized with REV to inhibit the miR-147 RNA level in DF-1 cells at 72hpi. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates.

    Techniques Used: Infection, Western Blot

    (A) ALV-J and REV synergistically enhanced the KIAA1199 RNA level in liver, kidney, bone marrow, bursa of Fabricius and heart of chicken at 60 dpi. Data represent mean ± SEM determined from three independent experiments (n = 6), each experiment containing three technical replicates. Compared with single-infection group: *P < 0.05 and **P < 0.01. (B) ALV-J synergized with REV to enhance the protein expression of KIAA1199 in kidney, heart and bone marrow in chicken at 60 dpi detected by immunohistochemical analysis with anti-KIAA1199 antibody. (C) Quantification of the results in (B). Compared with single-infection group: *P < 0.05 and **P < 0.01. (D) Co-infection of ALV-J and REV promoted the expression of KIAA1199 in fibroma of endocardium detected by immunohistochemical analysis with anti-KIAA1199 antibody. (E) The miR-147 expression was inhibited by co-infection of ALV-J and REV in kidney, bone marrow and heart, while that was increased in liver and bursa of Fabricius in chicken at 60 dpi. Data represent mean ± SEM determined from three independent experiments (n = 6), each experiment containing three technical replicates. Compared with single-infection group: *P < 0.05 and **P < 0.01.
    Figure Legend Snippet: (A) ALV-J and REV synergistically enhanced the KIAA1199 RNA level in liver, kidney, bone marrow, bursa of Fabricius and heart of chicken at 60 dpi. Data represent mean ± SEM determined from three independent experiments (n = 6), each experiment containing three technical replicates. Compared with single-infection group: *P < 0.05 and **P < 0.01. (B) ALV-J synergized with REV to enhance the protein expression of KIAA1199 in kidney, heart and bone marrow in chicken at 60 dpi detected by immunohistochemical analysis with anti-KIAA1199 antibody. (C) Quantification of the results in (B). Compared with single-infection group: *P < 0.05 and **P < 0.01. (D) Co-infection of ALV-J and REV promoted the expression of KIAA1199 in fibroma of endocardium detected by immunohistochemical analysis with anti-KIAA1199 antibody. (E) The miR-147 expression was inhibited by co-infection of ALV-J and REV in kidney, bone marrow and heart, while that was increased in liver and bursa of Fabricius in chicken at 60 dpi. Data represent mean ± SEM determined from three independent experiments (n = 6), each experiment containing three technical replicates. Compared with single-infection group: *P < 0.05 and **P < 0.01.

    Techniques Used: Infection, Expressing, Immunohistochemical staining

    (A) The RNA levels of NF-κB p65, KIAA1199 and EGFR were suppressed by incubating NF-κB p65 shRNA at 48hpi. Data represent mean ± SEM determined from three independent experiments (n=3), each experiment containing three technical replicates. (B) The chicken NF-κB p65 protein level was inhibited by NF-κB p65 shRNA detected by Chicken NF-κB p65 ELISA kit. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates. (C) The protein expression of KIAA1199 was decreased by NF-κB p65 shRNA at 48hpt detected by western blot with anti-KIAA1199 antibody. (D) The RNA level of KIAA1199, NF-κB p65 and EGFR were suppressed by KIAA1199 shRNA. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates. (E) The protein expression of KIAA1199 was decreased by KIAA1199 shRNA at 48h pt detected by western blot with anti-KIAA1199 antibody. (F) The protein level of chicken NF-κB p65 was inhibited by KIAA1199 shRNA detected by Chicken NF-κB p65 ELISA kit. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates.
    Figure Legend Snippet: (A) The RNA levels of NF-κB p65, KIAA1199 and EGFR were suppressed by incubating NF-κB p65 shRNA at 48hpi. Data represent mean ± SEM determined from three independent experiments (n=3), each experiment containing three technical replicates. (B) The chicken NF-κB p65 protein level was inhibited by NF-κB p65 shRNA detected by Chicken NF-κB p65 ELISA kit. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates. (C) The protein expression of KIAA1199 was decreased by NF-κB p65 shRNA at 48hpt detected by western blot with anti-KIAA1199 antibody. (D) The RNA level of KIAA1199, NF-κB p65 and EGFR were suppressed by KIAA1199 shRNA. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates. (E) The protein expression of KIAA1199 was decreased by KIAA1199 shRNA at 48h pt detected by western blot with anti-KIAA1199 antibody. (F) The protein level of chicken NF-κB p65 was inhibited by KIAA1199 shRNA detected by Chicken NF-κB p65 ELISA kit. Data represent mean ± SEM determined from three independent experiments (n = 3), each experiment containing three technical replicates.

    Techniques Used: shRNA, Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

    (A) MiR-147 inhibited the reporter activity of the pmirGLO-KIAA1199 3’UTR. MiR-147 mimics (40 nM) or negative control was co-transfected with pmirGLO-Control or pmirGLO-KIAA1199 3’UTR reporter plasmid into 293T cells. (B) MiR-147 mimics (10, 20 and 40 nM) or a negative control was co-transfected along with pmir-GL0-KIAA1199 3’UTR reporter plasmid into 293T cells. (C) MiR-147 inhibited expressions of KIAA1199 and NF-κB p50 in a dose-dependent manner. MiR-147 mimics (20 and 40 nM) were transfected into ALV-J and REV co-infected CEF, western blot was performed with anti-KIAA1199 antibody or anti-NF-κB p50 antibody at 48 h post-transfection. (D) Inhibition of miR-147 promoted expression of KIAA1199 and NF-κB p50. MiR-147 inhibitors (30 and 60 nM) were transfected into CEF and western blotting was performed with anti-KIAA1199 or anti-NF-κB p50 antibody at 48 h post-transfection. (E) Schematic diagram of predicted seed sequence of miR-147 which binds with KIAA1199 3’UTR. (F) KIAA1199 3’UTR wild type (WT KIAA1199) was co-transfected with a negative control (Neg. Ctrl.) or miR-147 into 293T cells, while mutant KIAA1199 3’UTR construct (mut KIAA1199) was also co-transfected with Neg. Ctrl. or miR-147. (G) Schematic diagram of predicted seed sequence of miR-147 which binds with NF-κB p50 3’UTR. (H) MiR-147 inhibited the reporter activity of the pmirGLO-NF-κB p50 3’UTR. MiR-147 mimics (40 nM) or negative control with pmirGLO-Control or pmirGLO-NF-κB p50 3’UTR reporter plasmid were cotransfected into 293T cells. (I) MiR-147 mimics (10, 20 and 40 nM) or a negative control was co-transfected into 293T cells along with pmir-GL0-NF-κB p50 3’UTR reporter plasmid. (J) NF-κB p50 3’UTR wild type (WT KIAA1199) was co-transfected with a negative control (Neg. Ctrl.) or miR-147 into 293T cells, while mutant NF-κB p50 3’UTR construct (mut NF-κB p50) was also co-transfected with Neg. Ctrl. or miR-147. All above Luciferase assays were performed 48 h later, data represent the mean ± SEM from three independent experiments (n = 3), and each experiment containing three technical replicates. **P < 0.01 by Student’s t test versus the Neg. Ctrl. group. n.s., not signifcant.
    Figure Legend Snippet: (A) MiR-147 inhibited the reporter activity of the pmirGLO-KIAA1199 3’UTR. MiR-147 mimics (40 nM) or negative control was co-transfected with pmirGLO-Control or pmirGLO-KIAA1199 3’UTR reporter plasmid into 293T cells. (B) MiR-147 mimics (10, 20 and 40 nM) or a negative control was co-transfected along with pmir-GL0-KIAA1199 3’UTR reporter plasmid into 293T cells. (C) MiR-147 inhibited expressions of KIAA1199 and NF-κB p50 in a dose-dependent manner. MiR-147 mimics (20 and 40 nM) were transfected into ALV-J and REV co-infected CEF, western blot was performed with anti-KIAA1199 antibody or anti-NF-κB p50 antibody at 48 h post-transfection. (D) Inhibition of miR-147 promoted expression of KIAA1199 and NF-κB p50. MiR-147 inhibitors (30 and 60 nM) were transfected into CEF and western blotting was performed with anti-KIAA1199 or anti-NF-κB p50 antibody at 48 h post-transfection. (E) Schematic diagram of predicted seed sequence of miR-147 which binds with KIAA1199 3’UTR. (F) KIAA1199 3’UTR wild type (WT KIAA1199) was co-transfected with a negative control (Neg. Ctrl.) or miR-147 into 293T cells, while mutant KIAA1199 3’UTR construct (mut KIAA1199) was also co-transfected with Neg. Ctrl. or miR-147. (G) Schematic diagram of predicted seed sequence of miR-147 which binds with NF-κB p50 3’UTR. (H) MiR-147 inhibited the reporter activity of the pmirGLO-NF-κB p50 3’UTR. MiR-147 mimics (40 nM) or negative control with pmirGLO-Control or pmirGLO-NF-κB p50 3’UTR reporter plasmid were cotransfected into 293T cells. (I) MiR-147 mimics (10, 20 and 40 nM) or a negative control was co-transfected into 293T cells along with pmir-GL0-NF-κB p50 3’UTR reporter plasmid. (J) NF-κB p50 3’UTR wild type (WT KIAA1199) was co-transfected with a negative control (Neg. Ctrl.) or miR-147 into 293T cells, while mutant NF-κB p50 3’UTR construct (mut NF-κB p50) was also co-transfected with Neg. Ctrl. or miR-147. All above Luciferase assays were performed 48 h later, data represent the mean ± SEM from three independent experiments (n = 3), and each experiment containing three technical replicates. **P < 0.01 by Student’s t test versus the Neg. Ctrl. group. n.s., not signifcant.

    Techniques Used: Activity Assay, Negative Control, Transfection, Plasmid Preparation, Infection, Western Blot, Inhibition, Expressing, Sequencing, Mutagenesis, Construct, Luciferase

    In ALV-J and REV co-infected cells, ALV-J synergizes with REV to further promote the NF-κB pathway. As a result, p50 and p65 were enhanced, leading to drive KIAA1199 gene transcription. KIAA1199 also activate EGFR signaling to promote NF-κB pathway stability. MiR-147, as a key to NF-κB/KIAA1199/EGFR pathway crosstalk, regulated p50, KIAA1199 and EGFR-driven cell-cycle proteins by targeting their 3’UTR region sequences, respectively, to further active the oncogene KIAA1199.
    Figure Legend Snippet: In ALV-J and REV co-infected cells, ALV-J synergizes with REV to further promote the NF-κB pathway. As a result, p50 and p65 were enhanced, leading to drive KIAA1199 gene transcription. KIAA1199 also activate EGFR signaling to promote NF-κB pathway stability. MiR-147, as a key to NF-κB/KIAA1199/EGFR pathway crosstalk, regulated p50, KIAA1199 and EGFR-driven cell-cycle proteins by targeting their 3’UTR region sequences, respectively, to further active the oncogene KIAA1199.

    Techniques Used: Infection



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