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polyclonal goat anti human c kit  (R&D Systems)


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    R&D Systems polyclonal goat anti human c kit
    Polyclonal Goat Anti Human C Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+scf+goat+ab/pmc06766656-98-38-44?v=R%26D+Systems
    Average 93 stars, based on 3 article reviews
    polyclonal goat anti human c kit - by Bioz Stars, 2026-07
    93/100 stars

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    A , KIT Y721 phosphorylation was activated by exogenous rhKITLG (100 ng/mL for 10 min following 2 h serum deprivation [ , ]) in GIST-T1 cells containing a heterozygous activating KIT mutation (n=4/group) and in GIST-T1-5R cells containing an additional, imatinib-resistant KIT mutation (n=6/group), but not in GIST882 cells lacking a WT KIT allele (n=5/group). B , Culturing with anti-human <t>KITLG</t> neutralizing antibody for 4 days inhibited baseline proliferation of GIST-T1 cells ( P <0.001; n=3; regression and 95% confidence band are shown as solid and dashed lines, respectively) and GIST-T1-5R cells ( P <0.001; n=6). The effect of KITLG immunoneutralization on GIST-T1 cells was blocked by preabsorbing the antibody with 10-fold molar excess of rhKITLG (see open symbols in the left panel, second row; n=3/group). KITLG immunoneutralization did not inhibit the proliferation of GIST882 or GIST48B cells lacking a WT KIT allele (note that GIST48B cells also express very low to undetectable levels of KIT protein, see ) and of LX-2 cells lacking KIT protein (n=3/cell line). C , Inhibition of the proliferation of GIST-T1 and GIST-T1-5R cells by siRNA-mediated knock-down of KITLG (n=4/cell line/group; P GIST-T1 : day 2: 0.008, days 4, 6 and 8: <0.001; P GIST-T1-5R : day 2: <0.02, day 4: 0.004, days 6 and 8: <0.001).
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    A , KIT Y721 phosphorylation was activated by exogenous rhKITLG (100 ng/mL for 10 min following 2 h serum deprivation [ , ]) in GIST-T1 cells containing a heterozygous activating KIT mutation (n=4/group) and in GIST-T1-5R cells containing an additional, imatinib-resistant KIT mutation (n=6/group), but not in GIST882 cells lacking a WT KIT allele (n=5/group). B , Culturing with anti-human <t>KITLG</t> neutralizing antibody for 4 days inhibited baseline proliferation of GIST-T1 cells ( P <0.001; n=3; regression and 95% confidence band are shown as solid and dashed lines, respectively) and GIST-T1-5R cells ( P <0.001; n=6). The effect of KITLG immunoneutralization on GIST-T1 cells was blocked by preabsorbing the antibody with 10-fold molar excess of rhKITLG (see open symbols in the left panel, second row; n=3/group). KITLG immunoneutralization did not inhibit the proliferation of GIST882 or GIST48B cells lacking a WT KIT allele (note that GIST48B cells also express very low to undetectable levels of KIT protein, see ) and of LX-2 cells lacking KIT protein (n=3/cell line). C , Inhibition of the proliferation of GIST-T1 and GIST-T1-5R cells by siRNA-mediated knock-down of KITLG (n=4/cell line/group; P GIST-T1 : day 2: 0.008, days 4, 6 and 8: <0.001; P GIST-T1-5R : day 2: <0.02, day 4: 0.004, days 6 and 8: <0.001).
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    A , KIT Y721 phosphorylation was activated by exogenous rhKITLG (100 ng/mL for 10 min following 2 h serum deprivation [ , ]) in GIST-T1 cells containing a heterozygous activating KIT mutation (n=4/group) and in GIST-T1-5R cells containing an additional, imatinib-resistant KIT mutation (n=6/group), but not in GIST882 cells lacking a WT KIT allele (n=5/group). B , Culturing with anti-human <t>KITLG</t> neutralizing antibody for 4 days inhibited baseline proliferation of GIST-T1 cells ( P <0.001; n=3; regression and 95% confidence band are shown as solid and dashed lines, respectively) and GIST-T1-5R cells ( P <0.001; n=6). The effect of KITLG immunoneutralization on GIST-T1 cells was blocked by preabsorbing the antibody with 10-fold molar excess of rhKITLG (see open symbols in the left panel, second row; n=3/group). KITLG immunoneutralization did not inhibit the proliferation of GIST882 or GIST48B cells lacking a WT KIT allele (note that GIST48B cells also express very low to undetectable levels of KIT protein, see ) and of LX-2 cells lacking KIT protein (n=3/cell line). C , Inhibition of the proliferation of GIST-T1 and GIST-T1-5R cells by siRNA-mediated knock-down of KITLG (n=4/cell line/group; P GIST-T1 : day 2: 0.008, days 4, 6 and 8: <0.001; P GIST-T1-5R : day 2: <0.02, day 4: 0.004, days 6 and 8: <0.001).
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    A , KIT Y721 phosphorylation was activated by exogenous rhKITLG (100 ng/mL for 10 min following 2 h serum deprivation [ , ]) in GIST-T1 cells containing a heterozygous activating KIT mutation (n=4/group) and in GIST-T1-5R cells containing an additional, imatinib-resistant KIT mutation (n=6/group), but not in GIST882 cells lacking a WT KIT allele (n=5/group). B , Culturing with anti-human <t>KITLG</t> neutralizing antibody for 4 days inhibited baseline proliferation of GIST-T1 cells ( P <0.001; n=3; regression and 95% confidence band are shown as solid and dashed lines, respectively) and GIST-T1-5R cells ( P <0.001; n=6). The effect of KITLG immunoneutralization on GIST-T1 cells was blocked by preabsorbing the antibody with 10-fold molar excess of rhKITLG (see open symbols in the left panel, second row; n=3/group). KITLG immunoneutralization did not inhibit the proliferation of GIST882 or GIST48B cells lacking a WT KIT allele (note that GIST48B cells also express very low to undetectable levels of KIT protein, see ) and of LX-2 cells lacking KIT protein (n=3/cell line). C , Inhibition of the proliferation of GIST-T1 and GIST-T1-5R cells by siRNA-mediated knock-down of KITLG (n=4/cell line/group; P GIST-T1 : day 2: 0.008, days 4, 6 and 8: <0.001; P GIST-T1-5R : day 2: <0.02, day 4: 0.004, days 6 and 8: <0.001).
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    goat polyclonal anti human stem cell factor scf  (R&D Systems)
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    A , KIT Y721 phosphorylation was activated by exogenous rhKITLG (100 ng/mL for 10 min following 2 h serum deprivation [ , ]) in GIST-T1 cells containing a heterozygous activating KIT mutation (n=4/group) and in GIST-T1-5R cells containing an additional, imatinib-resistant KIT mutation (n=6/group), but not in GIST882 cells lacking a WT KIT allele (n=5/group). B , Culturing with anti-human <t>KITLG</t> neutralizing antibody for 4 days inhibited baseline proliferation of GIST-T1 cells ( P <0.001; n=3; regression and 95% confidence band are shown as solid and dashed lines, respectively) and GIST-T1-5R cells ( P <0.001; n=6). The effect of KITLG immunoneutralization on GIST-T1 cells was blocked by preabsorbing the antibody with 10-fold molar excess of rhKITLG (see open symbols in the left panel, second row; n=3/group). KITLG immunoneutralization did not inhibit the proliferation of GIST882 or GIST48B cells lacking a WT KIT allele (note that GIST48B cells also express very low to undetectable levels of KIT protein, see ) and of LX-2 cells lacking KIT protein (n=3/cell line). C , Inhibition of the proliferation of GIST-T1 and GIST-T1-5R cells by siRNA-mediated knock-down of KITLG (n=4/cell line/group; P GIST-T1 : day 2: 0.008, days 4, 6 and 8: <0.001; P GIST-T1-5R : day 2: <0.02, day 4: 0.004, days 6 and 8: <0.001).
    Goat Polyclonal Anti Human Stem Cell Factor Scf, supplied by R&D Systems, 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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    A , KIT Y721 phosphorylation was activated by exogenous rhKITLG (100 ng/mL for 10 min following 2 h serum deprivation [ , ]) in GIST-T1 cells containing a heterozygous activating KIT mutation (n=4/group) and in GIST-T1-5R cells containing an additional, imatinib-resistant KIT mutation (n=6/group), but not in GIST882 cells lacking a WT KIT allele (n=5/group). B , Culturing with anti-human KITLG neutralizing antibody for 4 days inhibited baseline proliferation of GIST-T1 cells ( P <0.001; n=3; regression and 95% confidence band are shown as solid and dashed lines, respectively) and GIST-T1-5R cells ( P <0.001; n=6). The effect of KITLG immunoneutralization on GIST-T1 cells was blocked by preabsorbing the antibody with 10-fold molar excess of rhKITLG (see open symbols in the left panel, second row; n=3/group). KITLG immunoneutralization did not inhibit the proliferation of GIST882 or GIST48B cells lacking a WT KIT allele (note that GIST48B cells also express very low to undetectable levels of KIT protein, see ) and of LX-2 cells lacking KIT protein (n=3/cell line). C , Inhibition of the proliferation of GIST-T1 and GIST-T1-5R cells by siRNA-mediated knock-down of KITLG (n=4/cell line/group; P GIST-T1 : day 2: 0.008, days 4, 6 and 8: <0.001; P GIST-T1-5R : day 2: <0.02, day 4: 0.004, days 6 and 8: <0.001).

    Journal: PLoS ONE

    Article Title: Membrane-To-Nucleus Signaling Links Insulin-Like Growth Factor-1- and Stem Cell Factor-Activated Pathways

    doi: 10.1371/journal.pone.0076822

    Figure Lengend Snippet: A , KIT Y721 phosphorylation was activated by exogenous rhKITLG (100 ng/mL for 10 min following 2 h serum deprivation [ , ]) in GIST-T1 cells containing a heterozygous activating KIT mutation (n=4/group) and in GIST-T1-5R cells containing an additional, imatinib-resistant KIT mutation (n=6/group), but not in GIST882 cells lacking a WT KIT allele (n=5/group). B , Culturing with anti-human KITLG neutralizing antibody for 4 days inhibited baseline proliferation of GIST-T1 cells ( P <0.001; n=3; regression and 95% confidence band are shown as solid and dashed lines, respectively) and GIST-T1-5R cells ( P <0.001; n=6). The effect of KITLG immunoneutralization on GIST-T1 cells was blocked by preabsorbing the antibody with 10-fold molar excess of rhKITLG (see open symbols in the left panel, second row; n=3/group). KITLG immunoneutralization did not inhibit the proliferation of GIST882 or GIST48B cells lacking a WT KIT allele (note that GIST48B cells also express very low to undetectable levels of KIT protein, see ) and of LX-2 cells lacking KIT protein (n=3/cell line). C , Inhibition of the proliferation of GIST-T1 and GIST-T1-5R cells by siRNA-mediated knock-down of KITLG (n=4/cell line/group; P GIST-T1 : day 2: 0.008, days 4, 6 and 8: <0.001; P GIST-T1-5R : day 2: <0.02, day 4: 0.004, days 6 and 8: <0.001).

    Article Snippet: The role of endogenous KITLG in the proliferation of GIST-T1, GIST-T1-5R, GIST882, GIST48B and LX-2 cells was tested by culturing in the above media in the presence of purified, azide-free goat polyclonal anti-human KITLG antibody (AB-255-NA, R&D Systems, Minneapolis, MN; applied for 4 days at concentrations indicated in the Results), which has been shown to neutralize KITLG-induced proliferation in the TF1 human erythroleukemic cell line [ ].

    Techniques: Phospho-proteomics, Mutagenesis, Inhibition, Knockdown

    Results obtained in murine and human smooth muscle cells ( A - E ), human LX-2 stellate cells ( F - G ) and human GIST-T1 cells ( H - I ) are shown. A , Hoffman modulation contrast image of primary human gastric smooth muscle cells. B , KITLG mRNA (total: soluble+membrane-bound) was readily detectable in primary human smooth muscle cells (passage 3) maintained with Smooth Muscle Growth Medium-2 containing insulin, hFGF-B, hEGF and 5% FBS (Lonza) but not in 24-h growth factor- and serum-deficient basal medium. C , Both IGF1 (100 ng/mL) and the GSK3α/β inhibitor SB415286 (30 µM) stimulated Kitl expression in murine gastric tunica muscularis organotypic cultures (n=3/group). D - E , SB415286 stimulated endogenous Kitl expression in murine primary gastric smooth muscle cells ( D ; n=3/group) and KITLG transcriptional activity in the same cell type transfected with a KITLG promoter (-2120 bp to +407 bp)-pGL3 luciferase construct ( E ; n=3/group). IGF1 (100 ng/mL; n=3/group) and SB415286 (30 µM; n=6/group) also increased endogenous KITLG mRNA expression in LX-2 ( F ) and GIST-T1 cells ( H ) and stimulated KITLG promoter activity in a time-dependent fashion (LX-2: n=6-9/group; G ; GIST-T1: n=3-11/group; I ). Groups marked by asterisk are different from the control group, and groups not sharing the same superscript letter are different from each other ( P <0.05 by post-hoc multiple comparisons).

    Journal: PLoS ONE

    Article Title: Membrane-To-Nucleus Signaling Links Insulin-Like Growth Factor-1- and Stem Cell Factor-Activated Pathways

    doi: 10.1371/journal.pone.0076822

    Figure Lengend Snippet: Results obtained in murine and human smooth muscle cells ( A - E ), human LX-2 stellate cells ( F - G ) and human GIST-T1 cells ( H - I ) are shown. A , Hoffman modulation contrast image of primary human gastric smooth muscle cells. B , KITLG mRNA (total: soluble+membrane-bound) was readily detectable in primary human smooth muscle cells (passage 3) maintained with Smooth Muscle Growth Medium-2 containing insulin, hFGF-B, hEGF and 5% FBS (Lonza) but not in 24-h growth factor- and serum-deficient basal medium. C , Both IGF1 (100 ng/mL) and the GSK3α/β inhibitor SB415286 (30 µM) stimulated Kitl expression in murine gastric tunica muscularis organotypic cultures (n=3/group). D - E , SB415286 stimulated endogenous Kitl expression in murine primary gastric smooth muscle cells ( D ; n=3/group) and KITLG transcriptional activity in the same cell type transfected with a KITLG promoter (-2120 bp to +407 bp)-pGL3 luciferase construct ( E ; n=3/group). IGF1 (100 ng/mL; n=3/group) and SB415286 (30 µM; n=6/group) also increased endogenous KITLG mRNA expression in LX-2 ( F ) and GIST-T1 cells ( H ) and stimulated KITLG promoter activity in a time-dependent fashion (LX-2: n=6-9/group; G ; GIST-T1: n=3-11/group; I ). Groups marked by asterisk are different from the control group, and groups not sharing the same superscript letter are different from each other ( P <0.05 by post-hoc multiple comparisons).

    Article Snippet: The role of endogenous KITLG in the proliferation of GIST-T1, GIST-T1-5R, GIST882, GIST48B and LX-2 cells was tested by culturing in the above media in the presence of purified, azide-free goat polyclonal anti-human KITLG antibody (AB-255-NA, R&D Systems, Minneapolis, MN; applied for 4 days at concentrations indicated in the Results), which has been shown to neutralize KITLG-induced proliferation in the TF1 human erythroleukemic cell line [ ].

    Techniques: Membrane, Expressing, Activity Assay, Transfection, Luciferase, Construct, Control

    A , Increased occupancy of the Kitl core promoter region by H4ac in response to 6-h rhIGF1 (100 ng/mL) and SB415286 (30 µM) treatment in murine gastric smooth muscles. Only SB415286 increased occupancy by H3K9ac ( B ). Representatives of two independent experiments, each performed in triplicates, are shown. C , Dose-dependent stimulation of KITLG expression in LX-2 cells by 24-h treatment with the class I-II HDAC inhibitor SAHA (n=3/group). D , Dose-dependent inhibition of the SB415286-induced stimulation of KITLG expression by the p300/PCAF HAT inhibitor garcinol (24 h) in LX-2 cells (n=3/group). Drugs were applied following 24-h serum deprivation. Groups marked by asterisk are different from the control group, and groups not sharing the same superscript letter are different from each other ( P <0.05 by post-hoc multiple comparisons).

    Journal: PLoS ONE

    Article Title: Membrane-To-Nucleus Signaling Links Insulin-Like Growth Factor-1- and Stem Cell Factor-Activated Pathways

    doi: 10.1371/journal.pone.0076822

    Figure Lengend Snippet: A , Increased occupancy of the Kitl core promoter region by H4ac in response to 6-h rhIGF1 (100 ng/mL) and SB415286 (30 µM) treatment in murine gastric smooth muscles. Only SB415286 increased occupancy by H3K9ac ( B ). Representatives of two independent experiments, each performed in triplicates, are shown. C , Dose-dependent stimulation of KITLG expression in LX-2 cells by 24-h treatment with the class I-II HDAC inhibitor SAHA (n=3/group). D , Dose-dependent inhibition of the SB415286-induced stimulation of KITLG expression by the p300/PCAF HAT inhibitor garcinol (24 h) in LX-2 cells (n=3/group). Drugs were applied following 24-h serum deprivation. Groups marked by asterisk are different from the control group, and groups not sharing the same superscript letter are different from each other ( P <0.05 by post-hoc multiple comparisons).

    Article Snippet: The role of endogenous KITLG in the proliferation of GIST-T1, GIST-T1-5R, GIST882, GIST48B and LX-2 cells was tested by culturing in the above media in the presence of purified, azide-free goat polyclonal anti-human KITLG antibody (AB-255-NA, R&D Systems, Minneapolis, MN; applied for 4 days at concentrations indicated in the Results), which has been shown to neutralize KITLG-induced proliferation in the TF1 human erythroleukemic cell line [ ].

    Techniques: Muscles, Expressing, Inhibition, Control

    A , Increased occupancy of the Kitl core promoter by the trithorax group-mediated, activating H3K4me2 histone modification in response to 6-h rhIGF1 (100 ng/mL) and SB415286 (30 µM) treatment in murine gastric smooth muscles. B - C , Reduced occupancy of the Kitl core promoter by the PRC2-mediated, repressive H3K27me3 histone modification ( B ) and by the PRC2 histone methyltransferase EZH2 ( C ) in response to rhIGF1 and SB415286 in the same tissues. D - F , Stimulation of KITLG expression by the indirect histone methyltransferase inhibitor Adox in murine gastric smooth muscles ( D ), LX-2 cells ( E ) and GIST-T1 cells ( F ) (n=3/group). Adox was applied for 72 h following 24-h serum deprivation. See further details in the legend to .

    Journal: PLoS ONE

    Article Title: Membrane-To-Nucleus Signaling Links Insulin-Like Growth Factor-1- and Stem Cell Factor-Activated Pathways

    doi: 10.1371/journal.pone.0076822

    Figure Lengend Snippet: A , Increased occupancy of the Kitl core promoter by the trithorax group-mediated, activating H3K4me2 histone modification in response to 6-h rhIGF1 (100 ng/mL) and SB415286 (30 µM) treatment in murine gastric smooth muscles. B - C , Reduced occupancy of the Kitl core promoter by the PRC2-mediated, repressive H3K27me3 histone modification ( B ) and by the PRC2 histone methyltransferase EZH2 ( C ) in response to rhIGF1 and SB415286 in the same tissues. D - F , Stimulation of KITLG expression by the indirect histone methyltransferase inhibitor Adox in murine gastric smooth muscles ( D ), LX-2 cells ( E ) and GIST-T1 cells ( F ) (n=3/group). Adox was applied for 72 h following 24-h serum deprivation. See further details in the legend to .

    Article Snippet: The role of endogenous KITLG in the proliferation of GIST-T1, GIST-T1-5R, GIST882, GIST48B and LX-2 cells was tested by culturing in the above media in the presence of purified, azide-free goat polyclonal anti-human KITLG antibody (AB-255-NA, R&D Systems, Minneapolis, MN; applied for 4 days at concentrations indicated in the Results), which has been shown to neutralize KITLG-induced proliferation in the TF1 human erythroleukemic cell line [ ].

    Techniques: Modification, Muscles, Expressing

    A - B , Reduced occupancy of the Kitl core promoter by the repressive H3K9me2 ( A ) and H3K9me3 ( B ) histone modifications in response to 6-h rhIGF1 (100 ng/mL) and SB415286 (30 µM) treatment in murine gastric smooth muscles. C - D , Probing the role of HP1 isoforms in transcriptional repression of KITLG in LX-2 cells by siRNA- (CBX5: HP1α; 25 nM, 72 h; C ) or shRNA-mediated knock-down (CBX1: HP1β; CBX3: HP1γ; 30 µg plasmid, 72 h; D ). Note activation of KITLG expression by shRNA-mediated knock-down of HP1γ (n=3/group). E - F , Stimulation of KITLG expression by the G9A/GLP H3K9me1/2 HKMT inhibitor BIX-01294 in LX-2 cells ( E ) and GIST-T1 cells ( F ) (n=3/group). G , Stimulation of KITLG expression by the H3K9 HKMT inhibitor chaetocin in LX-2 cells (n=3/group). Drugs were applied for 24 h following 24-h serum deprivation. See further details in the legend to .

    Journal: PLoS ONE

    Article Title: Membrane-To-Nucleus Signaling Links Insulin-Like Growth Factor-1- and Stem Cell Factor-Activated Pathways

    doi: 10.1371/journal.pone.0076822

    Figure Lengend Snippet: A - B , Reduced occupancy of the Kitl core promoter by the repressive H3K9me2 ( A ) and H3K9me3 ( B ) histone modifications in response to 6-h rhIGF1 (100 ng/mL) and SB415286 (30 µM) treatment in murine gastric smooth muscles. C - D , Probing the role of HP1 isoforms in transcriptional repression of KITLG in LX-2 cells by siRNA- (CBX5: HP1α; 25 nM, 72 h; C ) or shRNA-mediated knock-down (CBX1: HP1β; CBX3: HP1γ; 30 µg plasmid, 72 h; D ). Note activation of KITLG expression by shRNA-mediated knock-down of HP1γ (n=3/group). E - F , Stimulation of KITLG expression by the G9A/GLP H3K9me1/2 HKMT inhibitor BIX-01294 in LX-2 cells ( E ) and GIST-T1 cells ( F ) (n=3/group). G , Stimulation of KITLG expression by the H3K9 HKMT inhibitor chaetocin in LX-2 cells (n=3/group). Drugs were applied for 24 h following 24-h serum deprivation. See further details in the legend to .

    Article Snippet: The role of endogenous KITLG in the proliferation of GIST-T1, GIST-T1-5R, GIST882, GIST48B and LX-2 cells was tested by culturing in the above media in the presence of purified, azide-free goat polyclonal anti-human KITLG antibody (AB-255-NA, R&D Systems, Minneapolis, MN; applied for 4 days at concentrations indicated in the Results), which has been shown to neutralize KITLG-induced proliferation in the TF1 human erythroleukemic cell line [ ].

    Techniques: Muscles, shRNA, Knockdown, Plasmid Preparation, Activation Assay, Expressing