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flnb constructs  (Qiagen)


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    Structured Review

    Qiagen flnb constructs
    H-RAS-transformed <t>Flnb</t> -deficient fibroblasts form larger tumors in SCID mice. ( a ) Genotyping of wild-type ( Flnb +/+ ) and Flnb -deficient ( Flnb −/− ) <t>MEFs</t> <t>transfected</t> with plasmid encoding H-RAS. ( b ) Immunoblots of total RAS expression in Flnb +/+ and Flnb −/− cells transfected with plasmid encoding H-RAS (H-RAS + ) and nontransfected cells (H-RAS − ). ( c ) Number of Flnb −/− H-RAS + , Flnb +/+ H-RAS + and Flnb +/+ H-RAS − (wild-type) MEF cells assayed for proliferation. ( d ) Volume of Flnb −/− H-RAS + and Flnb +/+ H-RAS + tumors inoculated into SCID mice up to 13 days ( n =12 in each group). Data are expressed as mean±s.d. * P <0.05; *** P <0.001 versus Flnb +/+ H-RAS + cells or tumors.
    Flnb Constructs, supplied by Qiagen, 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/flnb constructs/product/Qiagen
    Average 90 stars, based on 1 article reviews
    flnb constructs - by Bioz Stars, 2026-02
    90/100 stars

    Images

    1) Product Images from "Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A"

    Article Title: Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A

    Journal: Oncogenesis

    doi: 10.1038/oncsis.2014.33

    H-RAS-transformed Flnb -deficient fibroblasts form larger tumors in SCID mice. ( a ) Genotyping of wild-type ( Flnb +/+ ) and Flnb -deficient ( Flnb −/− ) MEFs transfected with plasmid encoding H-RAS. ( b ) Immunoblots of total RAS expression in Flnb +/+ and Flnb −/− cells transfected with plasmid encoding H-RAS (H-RAS + ) and nontransfected cells (H-RAS − ). ( c ) Number of Flnb −/− H-RAS + , Flnb +/+ H-RAS + and Flnb +/+ H-RAS − (wild-type) MEF cells assayed for proliferation. ( d ) Volume of Flnb −/− H-RAS + and Flnb +/+ H-RAS + tumors inoculated into SCID mice up to 13 days ( n =12 in each group). Data are expressed as mean±s.d. * P <0.05; *** P <0.001 versus Flnb +/+ H-RAS + cells or tumors.
    Figure Legend Snippet: H-RAS-transformed Flnb -deficient fibroblasts form larger tumors in SCID mice. ( a ) Genotyping of wild-type ( Flnb +/+ ) and Flnb -deficient ( Flnb −/− ) MEFs transfected with plasmid encoding H-RAS. ( b ) Immunoblots of total RAS expression in Flnb +/+ and Flnb −/− cells transfected with plasmid encoding H-RAS (H-RAS + ) and nontransfected cells (H-RAS − ). ( c ) Number of Flnb −/− H-RAS + , Flnb +/+ H-RAS + and Flnb +/+ H-RAS − (wild-type) MEF cells assayed for proliferation. ( d ) Volume of Flnb −/− H-RAS + and Flnb +/+ H-RAS + tumors inoculated into SCID mice up to 13 days ( n =12 in each group). Data are expressed as mean±s.d. * P <0.05; *** P <0.001 versus Flnb +/+ H-RAS + cells or tumors.

    Techniques Used: Transformation Assay, Transfection, Plasmid Preparation, Western Blot, Expressing

    Increased MMP9 mRNA expression in vascular endothelial and tumor cells in the absence of FLNB. ( a ) Mmp9 mRNA expression in mouse embryonic filamin B-deficient ( Flnb −/− ) ECs as compared with wild-type ( Flnb +/+ ) ECs as detected by reverse transcriptase–PCR (RT–PCR). ( b ) FLNB protein expression in human melanoma M2 cells as detected by immunoblots after transfection with vector expressing FLNB shRNA. Immunoblot with Actin served as loading controls. Transfection with GFP shRNA was included as a negative control. ( c ) Increased mRNA expression of MMP9 in FLNB -silenced M2 cells. ( d ) FLNB protein expression in OVSCR8 cells transfected with FLNB shRNA, whereas same cells transfected with GFP shRNA served as negative controls. ( e ) Proteolytic activity of MMP-9 in human ovarian cancer OVSCR8 cells following transfection with FLNB or GFP shRNA. ( f ) Invasion of OVSCR8 cells after transfection with FLNB or GFP shRNA. Data of triplicated experiments are expressed as mean±s.d. * P <0.05; *** P <0.001 versu s respective controls.
    Figure Legend Snippet: Increased MMP9 mRNA expression in vascular endothelial and tumor cells in the absence of FLNB. ( a ) Mmp9 mRNA expression in mouse embryonic filamin B-deficient ( Flnb −/− ) ECs as compared with wild-type ( Flnb +/+ ) ECs as detected by reverse transcriptase–PCR (RT–PCR). ( b ) FLNB protein expression in human melanoma M2 cells as detected by immunoblots after transfection with vector expressing FLNB shRNA. Immunoblot with Actin served as loading controls. Transfection with GFP shRNA was included as a negative control. ( c ) Increased mRNA expression of MMP9 in FLNB -silenced M2 cells. ( d ) FLNB protein expression in OVSCR8 cells transfected with FLNB shRNA, whereas same cells transfected with GFP shRNA served as negative controls. ( e ) Proteolytic activity of MMP-9 in human ovarian cancer OVSCR8 cells following transfection with FLNB or GFP shRNA. ( f ) Invasion of OVSCR8 cells after transfection with FLNB or GFP shRNA. Data of triplicated experiments are expressed as mean±s.d. * P <0.05; *** P <0.001 versu s respective controls.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Transfection, Plasmid Preparation, shRNA, Negative Control, Activity Assay

    Increased intratumor vascularity because of increased VEGF-A secretion in Flnb -deficient tumors in vivo . ( a ) Micrographs of vascular networks within mouse tumors formed by H-RAS-transformed MEFs. Red color represents PECAM-positive endothelial cells (scale bar, 100 μm). ( b ) Secreted levels of VEGF-A in mouse H-RAS-transformed wild-type ( Flnb +/+ H-RAS + ) or homozygous Flnb -deficient ( Flnb −/− H-RAS + ) tumors. ( c ) Secreted levels of VEGF-A in wild-type ( Flnb +/+ ) and homozygous Flnb -deficient ( Flnb −/− ) MEFs treated without reagent (Ø), PMA or MAPK inhibitor. ( d ) Secreted levels of VEGF in OVSCR8 cells following transfection with FLNB or GFP shRNA. ( e ) Representative image and quantification of circular vascular structures of porcine aortic endothelial (PAE) cells after conditioning with conditioned medium from FLNB or GFP shRNA-transfected OVSCR8 cells. Data of triplicate or quadruplicate experiments are expressed as mean±s.d. * P <0.05, ** P <0.01 and *** P <0.001 versus respective controls.
    Figure Legend Snippet: Increased intratumor vascularity because of increased VEGF-A secretion in Flnb -deficient tumors in vivo . ( a ) Micrographs of vascular networks within mouse tumors formed by H-RAS-transformed MEFs. Red color represents PECAM-positive endothelial cells (scale bar, 100 μm). ( b ) Secreted levels of VEGF-A in mouse H-RAS-transformed wild-type ( Flnb +/+ H-RAS + ) or homozygous Flnb -deficient ( Flnb −/− H-RAS + ) tumors. ( c ) Secreted levels of VEGF-A in wild-type ( Flnb +/+ ) and homozygous Flnb -deficient ( Flnb −/− ) MEFs treated without reagent (Ø), PMA or MAPK inhibitor. ( d ) Secreted levels of VEGF in OVSCR8 cells following transfection with FLNB or GFP shRNA. ( e ) Representative image and quantification of circular vascular structures of porcine aortic endothelial (PAE) cells after conditioning with conditioned medium from FLNB or GFP shRNA-transfected OVSCR8 cells. Data of triplicate or quadruplicate experiments are expressed as mean±s.d. * P <0.05, ** P <0.01 and *** P <0.001 versus respective controls.

    Techniques Used: In Vivo, Transformation Assay, Transfection, shRNA



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    Qiagen flnb constructs
    H-RAS-transformed <t>Flnb</t> -deficient fibroblasts form larger tumors in SCID mice. ( a ) Genotyping of wild-type ( Flnb +/+ ) and Flnb -deficient ( Flnb −/− ) <t>MEFs</t> <t>transfected</t> with plasmid encoding H-RAS. ( b ) Immunoblots of total RAS expression in Flnb +/+ and Flnb −/− cells transfected with plasmid encoding H-RAS (H-RAS + ) and nontransfected cells (H-RAS − ). ( c ) Number of Flnb −/− H-RAS + , Flnb +/+ H-RAS + and Flnb +/+ H-RAS − (wild-type) MEF cells assayed for proliferation. ( d ) Volume of Flnb −/− H-RAS + and Flnb +/+ H-RAS + tumors inoculated into SCID mice up to 13 days ( n =12 in each group). Data are expressed as mean±s.d. * P <0.05; *** P <0.001 versus Flnb +/+ H-RAS + cells or tumors.
    Flnb Constructs, supplied by Qiagen, 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/flnb constructs/product/Qiagen
    Average 90 stars, based on 1 article reviews
    flnb constructs - by Bioz Stars, 2026-02
    90/100 stars
      Buy from Supplier

    Image Search Results


    H-RAS-transformed Flnb -deficient fibroblasts form larger tumors in SCID mice. ( a ) Genotyping of wild-type ( Flnb +/+ ) and Flnb -deficient ( Flnb −/− ) MEFs transfected with plasmid encoding H-RAS. ( b ) Immunoblots of total RAS expression in Flnb +/+ and Flnb −/− cells transfected with plasmid encoding H-RAS (H-RAS + ) and nontransfected cells (H-RAS − ). ( c ) Number of Flnb −/− H-RAS + , Flnb +/+ H-RAS + and Flnb +/+ H-RAS − (wild-type) MEF cells assayed for proliferation. ( d ) Volume of Flnb −/− H-RAS + and Flnb +/+ H-RAS + tumors inoculated into SCID mice up to 13 days ( n =12 in each group). Data are expressed as mean±s.d. * P <0.05; *** P <0.001 versus Flnb +/+ H-RAS + cells or tumors.

    Journal: Oncogenesis

    Article Title: Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A

    doi: 10.1038/oncsis.2014.33

    Figure Lengend Snippet: H-RAS-transformed Flnb -deficient fibroblasts form larger tumors in SCID mice. ( a ) Genotyping of wild-type ( Flnb +/+ ) and Flnb -deficient ( Flnb −/− ) MEFs transfected with plasmid encoding H-RAS. ( b ) Immunoblots of total RAS expression in Flnb +/+ and Flnb −/− cells transfected with plasmid encoding H-RAS (H-RAS + ) and nontransfected cells (H-RAS − ). ( c ) Number of Flnb −/− H-RAS + , Flnb +/+ H-RAS + and Flnb +/+ H-RAS − (wild-type) MEF cells assayed for proliferation. ( d ) Volume of Flnb −/− H-RAS + and Flnb +/+ H-RAS + tumors inoculated into SCID mice up to 13 days ( n =12 in each group). Data are expressed as mean±s.d. * P <0.05; *** P <0.001 versus Flnb +/+ H-RAS + cells or tumors.

    Article Snippet: M2, A7 and OVSCR-8 cells were transfected with either shRNA GFP or FLNB constructs (SA Biosciences, Frederick, MD, USA) using Fugene HD transfection reagent according to the manufacturer's protocol (Promega, Madison, WI, USA).

    Techniques: Transformation Assay, Transfection, Plasmid Preparation, Western Blot, Expressing

    Increased MMP9 mRNA expression in vascular endothelial and tumor cells in the absence of FLNB. ( a ) Mmp9 mRNA expression in mouse embryonic filamin B-deficient ( Flnb −/− ) ECs as compared with wild-type ( Flnb +/+ ) ECs as detected by reverse transcriptase–PCR (RT–PCR). ( b ) FLNB protein expression in human melanoma M2 cells as detected by immunoblots after transfection with vector expressing FLNB shRNA. Immunoblot with Actin served as loading controls. Transfection with GFP shRNA was included as a negative control. ( c ) Increased mRNA expression of MMP9 in FLNB -silenced M2 cells. ( d ) FLNB protein expression in OVSCR8 cells transfected with FLNB shRNA, whereas same cells transfected with GFP shRNA served as negative controls. ( e ) Proteolytic activity of MMP-9 in human ovarian cancer OVSCR8 cells following transfection with FLNB or GFP shRNA. ( f ) Invasion of OVSCR8 cells after transfection with FLNB or GFP shRNA. Data of triplicated experiments are expressed as mean±s.d. * P <0.05; *** P <0.001 versu s respective controls.

    Journal: Oncogenesis

    Article Title: Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A

    doi: 10.1038/oncsis.2014.33

    Figure Lengend Snippet: Increased MMP9 mRNA expression in vascular endothelial and tumor cells in the absence of FLNB. ( a ) Mmp9 mRNA expression in mouse embryonic filamin B-deficient ( Flnb −/− ) ECs as compared with wild-type ( Flnb +/+ ) ECs as detected by reverse transcriptase–PCR (RT–PCR). ( b ) FLNB protein expression in human melanoma M2 cells as detected by immunoblots after transfection with vector expressing FLNB shRNA. Immunoblot with Actin served as loading controls. Transfection with GFP shRNA was included as a negative control. ( c ) Increased mRNA expression of MMP9 in FLNB -silenced M2 cells. ( d ) FLNB protein expression in OVSCR8 cells transfected with FLNB shRNA, whereas same cells transfected with GFP shRNA served as negative controls. ( e ) Proteolytic activity of MMP-9 in human ovarian cancer OVSCR8 cells following transfection with FLNB or GFP shRNA. ( f ) Invasion of OVSCR8 cells after transfection with FLNB or GFP shRNA. Data of triplicated experiments are expressed as mean±s.d. * P <0.05; *** P <0.001 versu s respective controls.

    Article Snippet: M2, A7 and OVSCR-8 cells were transfected with either shRNA GFP or FLNB constructs (SA Biosciences, Frederick, MD, USA) using Fugene HD transfection reagent according to the manufacturer's protocol (Promega, Madison, WI, USA).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Transfection, Plasmid Preparation, shRNA, Negative Control, Activity Assay

    Increased intratumor vascularity because of increased VEGF-A secretion in Flnb -deficient tumors in vivo . ( a ) Micrographs of vascular networks within mouse tumors formed by H-RAS-transformed MEFs. Red color represents PECAM-positive endothelial cells (scale bar, 100 μm). ( b ) Secreted levels of VEGF-A in mouse H-RAS-transformed wild-type ( Flnb +/+ H-RAS + ) or homozygous Flnb -deficient ( Flnb −/− H-RAS + ) tumors. ( c ) Secreted levels of VEGF-A in wild-type ( Flnb +/+ ) and homozygous Flnb -deficient ( Flnb −/− ) MEFs treated without reagent (Ø), PMA or MAPK inhibitor. ( d ) Secreted levels of VEGF in OVSCR8 cells following transfection with FLNB or GFP shRNA. ( e ) Representative image and quantification of circular vascular structures of porcine aortic endothelial (PAE) cells after conditioning with conditioned medium from FLNB or GFP shRNA-transfected OVSCR8 cells. Data of triplicate or quadruplicate experiments are expressed as mean±s.d. * P <0.05, ** P <0.01 and *** P <0.001 versus respective controls.

    Journal: Oncogenesis

    Article Title: Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A

    doi: 10.1038/oncsis.2014.33

    Figure Lengend Snippet: Increased intratumor vascularity because of increased VEGF-A secretion in Flnb -deficient tumors in vivo . ( a ) Micrographs of vascular networks within mouse tumors formed by H-RAS-transformed MEFs. Red color represents PECAM-positive endothelial cells (scale bar, 100 μm). ( b ) Secreted levels of VEGF-A in mouse H-RAS-transformed wild-type ( Flnb +/+ H-RAS + ) or homozygous Flnb -deficient ( Flnb −/− H-RAS + ) tumors. ( c ) Secreted levels of VEGF-A in wild-type ( Flnb +/+ ) and homozygous Flnb -deficient ( Flnb −/− ) MEFs treated without reagent (Ø), PMA or MAPK inhibitor. ( d ) Secreted levels of VEGF in OVSCR8 cells following transfection with FLNB or GFP shRNA. ( e ) Representative image and quantification of circular vascular structures of porcine aortic endothelial (PAE) cells after conditioning with conditioned medium from FLNB or GFP shRNA-transfected OVSCR8 cells. Data of triplicate or quadruplicate experiments are expressed as mean±s.d. * P <0.05, ** P <0.01 and *** P <0.001 versus respective controls.

    Article Snippet: M2, A7 and OVSCR-8 cells were transfected with either shRNA GFP or FLNB constructs (SA Biosciences, Frederick, MD, USA) using Fugene HD transfection reagent according to the manufacturer's protocol (Promega, Madison, WI, USA).

    Techniques: In Vivo, Transformation Assay, Transfection, shRNA