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rabbit anti-human tyro3  (Novus Biologicals)


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    Novus Biologicals rabbit anti-human tyro3
    A ) Representative dot plots showing the three main sub-populations of mononuclear cells based on the expression of CD11b, CD4, and CD1c. <t>TYRO3,</t> AXL, and MERTK expression were evaluated in circulating monocytes (CD11b high CD4 mid ) and DCs (CD1c high CD11b low ) of patients with MS, patients with HIMS, and healthy controls by flow cytometry. B-G ) The percentage of TYRO3-positive as well as the mean fluorescent intensity (MFI) of the receptor on monocytes ( B, C, and D ) and DCs ( E, F, and G ) are graphed. H, I, and J ) The percentage of AXL high as well as the MFI of the receptor on DCs are shown. K, L, and M ) The expression of MERTK on DCs is shown as both percentage and MFI. N, O, and P ) The percentage of circulating CD4 + T cell expressing GAS6 as well as its MFI are shown. Q, R, and S ) The percentage of circulating CD4 + T cell expressing PROS1 and its MFI are shown. Data is presented as a pool of independent samples included in the specific staining (Control N = 21–31; MS N = 10–27; and HIMS N = 11–16). One-way ANOVA with a Fisher post hoc test was performed to determine statistical significances, *p<0.05 **p≤0.01 ****p≤0.001. MS = multiple sclerosis, HIMS = helminth-infected multiple sclerosis.
    Rabbit Anti Human Tyro3, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 90 stars, based on 1 article reviews
    rabbit anti-human tyro3 - by Bioz Stars, 2026-02
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    Images

    1) Product Images from "GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection"

    Article Title: GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection

    Journal: PLoS Pathogens

    doi: 10.1371/journal.ppat.1009176

    A ) Representative dot plots showing the three main sub-populations of mononuclear cells based on the expression of CD11b, CD4, and CD1c. TYRO3, AXL, and MERTK expression were evaluated in circulating monocytes (CD11b high CD4 mid ) and DCs (CD1c high CD11b low ) of patients with MS, patients with HIMS, and healthy controls by flow cytometry. B-G ) The percentage of TYRO3-positive as well as the mean fluorescent intensity (MFI) of the receptor on monocytes ( B, C, and D ) and DCs ( E, F, and G ) are graphed. H, I, and J ) The percentage of AXL high as well as the MFI of the receptor on DCs are shown. K, L, and M ) The expression of MERTK on DCs is shown as both percentage and MFI. N, O, and P ) The percentage of circulating CD4 + T cell expressing GAS6 as well as its MFI are shown. Q, R, and S ) The percentage of circulating CD4 + T cell expressing PROS1 and its MFI are shown. Data is presented as a pool of independent samples included in the specific staining (Control N = 21–31; MS N = 10–27; and HIMS N = 11–16). One-way ANOVA with a Fisher post hoc test was performed to determine statistical significances, *p<0.05 **p≤0.01 ****p≤0.001. MS = multiple sclerosis, HIMS = helminth-infected multiple sclerosis.
    Figure Legend Snippet: A ) Representative dot plots showing the three main sub-populations of mononuclear cells based on the expression of CD11b, CD4, and CD1c. TYRO3, AXL, and MERTK expression were evaluated in circulating monocytes (CD11b high CD4 mid ) and DCs (CD1c high CD11b low ) of patients with MS, patients with HIMS, and healthy controls by flow cytometry. B-G ) The percentage of TYRO3-positive as well as the mean fluorescent intensity (MFI) of the receptor on monocytes ( B, C, and D ) and DCs ( E, F, and G ) are graphed. H, I, and J ) The percentage of AXL high as well as the MFI of the receptor on DCs are shown. K, L, and M ) The expression of MERTK on DCs is shown as both percentage and MFI. N, O, and P ) The percentage of circulating CD4 + T cell expressing GAS6 as well as its MFI are shown. Q, R, and S ) The percentage of circulating CD4 + T cell expressing PROS1 and its MFI are shown. Data is presented as a pool of independent samples included in the specific staining (Control N = 21–31; MS N = 10–27; and HIMS N = 11–16). One-way ANOVA with a Fisher post hoc test was performed to determine statistical significances, *p<0.05 **p≤0.01 ****p≤0.001. MS = multiple sclerosis, HIMS = helminth-infected multiple sclerosis.

    Techniques Used: Expressing, Flow Cytometry, Staining, Control, Infection

    The host type 2 immune response is elicited to clear parasitic helminth infections; however, the co-evolution of these parasites has promoted a variety of mechanisms to oppose and redirect immune responses by manipulating immune cell programming and function. Integrating our results with the current knowledge, we propose that gastrointestinal ( 1 ) helminths infections can enhance the regulatory axis of TAM receptors (TYRO3, AXL, and MERTK) in peripheral blood ( 2 ) CD11b high and CD1c high cells, and their ligand GAS6 in CD4 + T cells of patients with MS. This negative regulatory pathway could be essential for dampening co-stimulatory signals (CD40, CD80, and CD86) of antigen-presenting cells and controlling the pathological Th17 (pTh17) response at secondary lymphoid organs ( 3 ). The active chronic infection resets T helper response toward Th2/regulatory signals, limiting pathological Th17 (pTh17) effector response. This reprogramming of CD4 + T cells and GAS6 signaling under a helminth-induced type 2 environment could be essential for maintaining the balance between CD4 + IL-10 + and Th17 cells and reducing inflammatory IL-17 and IFNγ signals in the central nervous system ( 4 ). In summary, GAS6 tempers not only the innate immune response but also regulates Th17 development in an autocrine/paracrine manner.
    Figure Legend Snippet: The host type 2 immune response is elicited to clear parasitic helminth infections; however, the co-evolution of these parasites has promoted a variety of mechanisms to oppose and redirect immune responses by manipulating immune cell programming and function. Integrating our results with the current knowledge, we propose that gastrointestinal ( 1 ) helminths infections can enhance the regulatory axis of TAM receptors (TYRO3, AXL, and MERTK) in peripheral blood ( 2 ) CD11b high and CD1c high cells, and their ligand GAS6 in CD4 + T cells of patients with MS. This negative regulatory pathway could be essential for dampening co-stimulatory signals (CD40, CD80, and CD86) of antigen-presenting cells and controlling the pathological Th17 (pTh17) response at secondary lymphoid organs ( 3 ). The active chronic infection resets T helper response toward Th2/regulatory signals, limiting pathological Th17 (pTh17) effector response. This reprogramming of CD4 + T cells and GAS6 signaling under a helminth-induced type 2 environment could be essential for maintaining the balance between CD4 + IL-10 + and Th17 cells and reducing inflammatory IL-17 and IFNγ signals in the central nervous system ( 4 ). In summary, GAS6 tempers not only the innate immune response but also regulates Th17 development in an autocrine/paracrine manner.

    Techniques Used: Infection



    Similar Products

    rabbit anti-human tyro3  (Novus Biologicals)
    90
    Novus Biologicals rabbit anti-human tyro3
    A ) Representative dot plots showing the three main sub-populations of mononuclear cells based on the expression of CD11b, CD4, and CD1c. <t>TYRO3,</t> AXL, and MERTK expression were evaluated in circulating monocytes (CD11b high CD4 mid ) and DCs (CD1c high CD11b low ) of patients with MS, patients with HIMS, and healthy controls by flow cytometry. B-G ) The percentage of TYRO3-positive as well as the mean fluorescent intensity (MFI) of the receptor on monocytes ( B, C, and D ) and DCs ( E, F, and G ) are graphed. H, I, and J ) The percentage of AXL high as well as the MFI of the receptor on DCs are shown. K, L, and M ) The expression of MERTK on DCs is shown as both percentage and MFI. N, O, and P ) The percentage of circulating CD4 + T cell expressing GAS6 as well as its MFI are shown. Q, R, and S ) The percentage of circulating CD4 + T cell expressing PROS1 and its MFI are shown. Data is presented as a pool of independent samples included in the specific staining (Control N = 21–31; MS N = 10–27; and HIMS N = 11–16). One-way ANOVA with a Fisher post hoc test was performed to determine statistical significances, *p<0.05 **p≤0.01 ****p≤0.001. MS = multiple sclerosis, HIMS = helminth-infected multiple sclerosis.
    Rabbit Anti Human Tyro3, supplied by Novus Biologicals, 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/rabbit anti-human tyro3/product/Novus Biologicals
    Average 90 stars, based on 1 article reviews
    rabbit anti-human tyro3 - by Bioz Stars, 2026-02
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    primary antibodies against human tyro3  (Cell Signaling Technology Inc)
    95
    Cell Signaling Technology Inc primary antibodies against human tyro3
    Characterisation of TAM receptor expression in a panel of human LMS cell lines. ( A ) Lysates from IB112, IB118, IB133, IB134, IB136, SK-LMS-1 and HepG2 (positive control) were analysed by western blot. Beta-actin was used as loading control. Longer exposition is shown for HepG2 with AXL antibody. ( B ) Leiomyosarcoma cells were starved then stimulated with GAS6. After normalisation for protein concentration, phosphotyrosine proteins were immunoprecipitated with a PY20 antibody. The SK-LMS-1 lysate was immunoprecipitated also with an antibody isotype control. Western blot analysis was performed with an anti <t>TYRO3</t> antibody. ( C ) Graph showing AXL (red), MER (blue) and TYRO3 (green) expression levels in LMS and HepG2 cells by FACS analysis. Results are shown as fold increase compared to isotype control. ( D ) Evaluation of GAS6 levels in LMS cells lysates by ELISA.
    Primary Antibodies Against Human Tyro3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary antibodies against human tyro3/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    primary antibodies against human tyro3 - by Bioz Stars, 2026-02
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    Image Search Results


    A ) Representative dot plots showing the three main sub-populations of mononuclear cells based on the expression of CD11b, CD4, and CD1c. TYRO3, AXL, and MERTK expression were evaluated in circulating monocytes (CD11b high CD4 mid ) and DCs (CD1c high CD11b low ) of patients with MS, patients with HIMS, and healthy controls by flow cytometry. B-G ) The percentage of TYRO3-positive as well as the mean fluorescent intensity (MFI) of the receptor on monocytes ( B, C, and D ) and DCs ( E, F, and G ) are graphed. H, I, and J ) The percentage of AXL high as well as the MFI of the receptor on DCs are shown. K, L, and M ) The expression of MERTK on DCs is shown as both percentage and MFI. N, O, and P ) The percentage of circulating CD4 + T cell expressing GAS6 as well as its MFI are shown. Q, R, and S ) The percentage of circulating CD4 + T cell expressing PROS1 and its MFI are shown. Data is presented as a pool of independent samples included in the specific staining (Control N = 21–31; MS N = 10–27; and HIMS N = 11–16). One-way ANOVA with a Fisher post hoc test was performed to determine statistical significances, *p<0.05 **p≤0.01 ****p≤0.001. MS = multiple sclerosis, HIMS = helminth-infected multiple sclerosis.

    Journal: PLoS Pathogens

    Article Title: GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection

    doi: 10.1371/journal.ppat.1009176

    Figure Lengend Snippet: A ) Representative dot plots showing the three main sub-populations of mononuclear cells based on the expression of CD11b, CD4, and CD1c. TYRO3, AXL, and MERTK expression were evaluated in circulating monocytes (CD11b high CD4 mid ) and DCs (CD1c high CD11b low ) of patients with MS, patients with HIMS, and healthy controls by flow cytometry. B-G ) The percentage of TYRO3-positive as well as the mean fluorescent intensity (MFI) of the receptor on monocytes ( B, C, and D ) and DCs ( E, F, and G ) are graphed. H, I, and J ) The percentage of AXL high as well as the MFI of the receptor on DCs are shown. K, L, and M ) The expression of MERTK on DCs is shown as both percentage and MFI. N, O, and P ) The percentage of circulating CD4 + T cell expressing GAS6 as well as its MFI are shown. Q, R, and S ) The percentage of circulating CD4 + T cell expressing PROS1 and its MFI are shown. Data is presented as a pool of independent samples included in the specific staining (Control N = 21–31; MS N = 10–27; and HIMS N = 11–16). One-way ANOVA with a Fisher post hoc test was performed to determine statistical significances, *p<0.05 **p≤0.01 ****p≤0.001. MS = multiple sclerosis, HIMS = helminth-infected multiple sclerosis.

    Article Snippet: Rabbit anti-human TYRO3 (Novus Biological), biotin-conjugated goat anti-human AXL, and APC anti-human MERTK mAb IgG1 (R&D Systems) were used to evaluate TAM receptor expression after fixation and permeabilization (Cytofix/Cytoperm Kit, BD Bioscience, San Diego, CA, USA).

    Techniques: Expressing, Flow Cytometry, Staining, Control, Infection

    The host type 2 immune response is elicited to clear parasitic helminth infections; however, the co-evolution of these parasites has promoted a variety of mechanisms to oppose and redirect immune responses by manipulating immune cell programming and function. Integrating our results with the current knowledge, we propose that gastrointestinal ( 1 ) helminths infections can enhance the regulatory axis of TAM receptors (TYRO3, AXL, and MERTK) in peripheral blood ( 2 ) CD11b high and CD1c high cells, and their ligand GAS6 in CD4 + T cells of patients with MS. This negative regulatory pathway could be essential for dampening co-stimulatory signals (CD40, CD80, and CD86) of antigen-presenting cells and controlling the pathological Th17 (pTh17) response at secondary lymphoid organs ( 3 ). The active chronic infection resets T helper response toward Th2/regulatory signals, limiting pathological Th17 (pTh17) effector response. This reprogramming of CD4 + T cells and GAS6 signaling under a helminth-induced type 2 environment could be essential for maintaining the balance between CD4 + IL-10 + and Th17 cells and reducing inflammatory IL-17 and IFNγ signals in the central nervous system ( 4 ). In summary, GAS6 tempers not only the innate immune response but also regulates Th17 development in an autocrine/paracrine manner.

    Journal: PLoS Pathogens

    Article Title: GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection

    doi: 10.1371/journal.ppat.1009176

    Figure Lengend Snippet: The host type 2 immune response is elicited to clear parasitic helminth infections; however, the co-evolution of these parasites has promoted a variety of mechanisms to oppose and redirect immune responses by manipulating immune cell programming and function. Integrating our results with the current knowledge, we propose that gastrointestinal ( 1 ) helminths infections can enhance the regulatory axis of TAM receptors (TYRO3, AXL, and MERTK) in peripheral blood ( 2 ) CD11b high and CD1c high cells, and their ligand GAS6 in CD4 + T cells of patients with MS. This negative regulatory pathway could be essential for dampening co-stimulatory signals (CD40, CD80, and CD86) of antigen-presenting cells and controlling the pathological Th17 (pTh17) response at secondary lymphoid organs ( 3 ). The active chronic infection resets T helper response toward Th2/regulatory signals, limiting pathological Th17 (pTh17) effector response. This reprogramming of CD4 + T cells and GAS6 signaling under a helminth-induced type 2 environment could be essential for maintaining the balance between CD4 + IL-10 + and Th17 cells and reducing inflammatory IL-17 and IFNγ signals in the central nervous system ( 4 ). In summary, GAS6 tempers not only the innate immune response but also regulates Th17 development in an autocrine/paracrine manner.

    Article Snippet: Rabbit anti-human TYRO3 (Novus Biological), biotin-conjugated goat anti-human AXL, and APC anti-human MERTK mAb IgG1 (R&D Systems) were used to evaluate TAM receptor expression after fixation and permeabilization (Cytofix/Cytoperm Kit, BD Bioscience, San Diego, CA, USA).

    Techniques: Infection

    Characterisation of TAM receptor expression in a panel of human LMS cell lines. ( A ) Lysates from IB112, IB118, IB133, IB134, IB136, SK-LMS-1 and HepG2 (positive control) were analysed by western blot. Beta-actin was used as loading control. Longer exposition is shown for HepG2 with AXL antibody. ( B ) Leiomyosarcoma cells were starved then stimulated with GAS6. After normalisation for protein concentration, phosphotyrosine proteins were immunoprecipitated with a PY20 antibody. The SK-LMS-1 lysate was immunoprecipitated also with an antibody isotype control. Western blot analysis was performed with an anti TYRO3 antibody. ( C ) Graph showing AXL (red), MER (blue) and TYRO3 (green) expression levels in LMS and HepG2 cells by FACS analysis. Results are shown as fold increase compared to isotype control. ( D ) Evaluation of GAS6 levels in LMS cells lysates by ELISA.

    Journal: British Journal of Cancer

    Article Title: Expression and role of TYRO3 and AXL as potential therapeutical targets in leiomyosarcoma

    doi: 10.1038/bjc.2017.354

    Figure Lengend Snippet: Characterisation of TAM receptor expression in a panel of human LMS cell lines. ( A ) Lysates from IB112, IB118, IB133, IB134, IB136, SK-LMS-1 and HepG2 (positive control) were analysed by western blot. Beta-actin was used as loading control. Longer exposition is shown for HepG2 with AXL antibody. ( B ) Leiomyosarcoma cells were starved then stimulated with GAS6. After normalisation for protein concentration, phosphotyrosine proteins were immunoprecipitated with a PY20 antibody. The SK-LMS-1 lysate was immunoprecipitated also with an antibody isotype control. Western blot analysis was performed with an anti TYRO3 antibody. ( C ) Graph showing AXL (red), MER (blue) and TYRO3 (green) expression levels in LMS and HepG2 cells by FACS analysis. Results are shown as fold increase compared to isotype control. ( D ) Evaluation of GAS6 levels in LMS cells lysates by ELISA.

    Article Snippet: Primary antibodies against human TYRO3 (#5585; Cell Signalling, Saint Quentin Yvelines, France), AXL (ABN275; Millipore, Molsheim, France), phosphoAXL (Y779-AF2228; R&D Systems) and actin (A54441; Sigma-Aldrich) were used, followed by a secondary HRP-linked antibody.

    Techniques: Expressing, Positive Control, Western Blot, Control, Protein Concentration, Immunoprecipitation, Enzyme-linked Immunosorbent Assay

    (A) TYRO3 and AXL RTK protein expression following shRNA knockdown. SK-LMS-1 cells comprising TYRO3-targeting shRNA (sh1 and sh2), AXL-targeting shRNA (sh3 and sh4) and control shRNA (shPRPC) show TYRO3 and AXL levels by immunoblotting. (B) Knockdown of TYRO3 and AXL in the SK-LMS-1 cell line affects cell viability. Graph showing the reduction of viability in SK-LMS-1 knocked-down cells cultivated for 3 days. Viable cells were counted using trypan blue. Graphs represent means of two independent experiments performed in duplicates. (C) Graphs showing decrease in colony formation potential for SK-LMS-1 knockdown cells. Graphs represent means of two independent experiments performed in duplicates.

    Journal: British Journal of Cancer

    Article Title: Expression and role of TYRO3 and AXL as potential therapeutical targets in leiomyosarcoma

    doi: 10.1038/bjc.2017.354

    Figure Lengend Snippet: (A) TYRO3 and AXL RTK protein expression following shRNA knockdown. SK-LMS-1 cells comprising TYRO3-targeting shRNA (sh1 and sh2), AXL-targeting shRNA (sh3 and sh4) and control shRNA (shPRPC) show TYRO3 and AXL levels by immunoblotting. (B) Knockdown of TYRO3 and AXL in the SK-LMS-1 cell line affects cell viability. Graph showing the reduction of viability in SK-LMS-1 knocked-down cells cultivated for 3 days. Viable cells were counted using trypan blue. Graphs represent means of two independent experiments performed in duplicates. (C) Graphs showing decrease in colony formation potential for SK-LMS-1 knockdown cells. Graphs represent means of two independent experiments performed in duplicates.

    Article Snippet: Primary antibodies against human TYRO3 (#5585; Cell Signalling, Saint Quentin Yvelines, France), AXL (ABN275; Millipore, Molsheim, France), phosphoAXL (Y779-AF2228; R&D Systems) and actin (A54441; Sigma-Aldrich) were used, followed by a secondary HRP-linked antibody.

    Techniques: Expressing, shRNA, Knockdown, Control, Western Blot

    Crizotinib and foretinib deactivate TYRO3 and AXL phosphorylation and lead to decrease in cell viability. ( A ) Proteins with phosphorylated tyrosines were immunoprecipitated with a PY20 antibody from LMS cell lysates treated with crizotinib and foretinib. IB118 and SK-LMS-1 were precipitated also with an isotype control antibody, as shown in the right part of the panel. Western blot analysis was performed with an anti-TYRO3 and -AXL antibodies. Graphs showing TYRO3 ( B ) or AXL ( C ) protein quantification of western blot using ChemiDoc Imaging Systems (Bio-Rad). Leiomyosarcoma cells were treated with crizotinib ( D ) and foretinib ( E ) at indicated concentrations for 72 h. Viable cells were measured using CellTiterGlo (Promega) and plotted relative to untreated control. Graphs represent means of three independent experiments performed in triplicates. Bars represent s.d.’s.

    Journal: British Journal of Cancer

    Article Title: Expression and role of TYRO3 and AXL as potential therapeutical targets in leiomyosarcoma

    doi: 10.1038/bjc.2017.354

    Figure Lengend Snippet: Crizotinib and foretinib deactivate TYRO3 and AXL phosphorylation and lead to decrease in cell viability. ( A ) Proteins with phosphorylated tyrosines were immunoprecipitated with a PY20 antibody from LMS cell lysates treated with crizotinib and foretinib. IB118 and SK-LMS-1 were precipitated also with an isotype control antibody, as shown in the right part of the panel. Western blot analysis was performed with an anti-TYRO3 and -AXL antibodies. Graphs showing TYRO3 ( B ) or AXL ( C ) protein quantification of western blot using ChemiDoc Imaging Systems (Bio-Rad). Leiomyosarcoma cells were treated with crizotinib ( D ) and foretinib ( E ) at indicated concentrations for 72 h. Viable cells were measured using CellTiterGlo (Promega) and plotted relative to untreated control. Graphs represent means of three independent experiments performed in triplicates. Bars represent s.d.’s.

    Article Snippet: Primary antibodies against human TYRO3 (#5585; Cell Signalling, Saint Quentin Yvelines, France), AXL (ABN275; Millipore, Molsheim, France), phosphoAXL (Y779-AF2228; R&D Systems) and actin (A54441; Sigma-Aldrich) were used, followed by a secondary HRP-linked antibody.

    Techniques: Phospho-proteomics, Immunoprecipitation, Control, Western Blot, Imaging

    TYRO3, AXL and GAS6 expression in sarcomas. ( A ) Representative example of immunohistochemistry on LMS tissues with anti-AXL, anti-TYRO3 and anti-GAS6 antibodies. TYRO3 nuclear expression is shown in detail. Original magnification × 20 and × 40. ( B ) Graph showing the percentage of positive samples from each sarcoma hystotype analysed. Cytoplasmic or nuclear staining was plotted separately. ( C – F ) Gene expression analysis of TYRO3, AXL, GAS6 and PROS1 transcripts, respectively. Data are from gene expression and outcome in 251 sarcoma patients’ samples from ATGsarc microarray database. ( G ) Kaplan–Meier curve for progression-free survival of 94 LMS patients with low or mixed and high expression levels of GAS6 and PROS1 genes cluster. P -values in log-rank test are indicated. n =number of patients in each group. Median PFS are expressed in years.

    Journal: British Journal of Cancer

    Article Title: Expression and role of TYRO3 and AXL as potential therapeutical targets in leiomyosarcoma

    doi: 10.1038/bjc.2017.354

    Figure Lengend Snippet: TYRO3, AXL and GAS6 expression in sarcomas. ( A ) Representative example of immunohistochemistry on LMS tissues with anti-AXL, anti-TYRO3 and anti-GAS6 antibodies. TYRO3 nuclear expression is shown in detail. Original magnification × 20 and × 40. ( B ) Graph showing the percentage of positive samples from each sarcoma hystotype analysed. Cytoplasmic or nuclear staining was plotted separately. ( C – F ) Gene expression analysis of TYRO3, AXL, GAS6 and PROS1 transcripts, respectively. Data are from gene expression and outcome in 251 sarcoma patients’ samples from ATGsarc microarray database. ( G ) Kaplan–Meier curve for progression-free survival of 94 LMS patients with low or mixed and high expression levels of GAS6 and PROS1 genes cluster. P -values in log-rank test are indicated. n =number of patients in each group. Median PFS are expressed in years.

    Article Snippet: Primary antibodies against human TYRO3 (#5585; Cell Signalling, Saint Quentin Yvelines, France), AXL (ABN275; Millipore, Molsheim, France), phosphoAXL (Y779-AF2228; R&D Systems) and actin (A54441; Sigma-Aldrich) were used, followed by a secondary HRP-linked antibody.

    Techniques: Expressing, Immunohistochemistry, Staining, Gene Expression, Microarray