Review



antibodies against ddx23  (Bioss)


Bioz Verified Symbol Bioss is a verified supplier
Bioz Manufacturer Symbol Bioss manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 91
      Buy from Supplier

    Structured Review

    Bioss antibodies against ddx23
    a Scatter plot depicted SDC4 interactome. Log 2 heavy (H) / light (L) ratios of the quantified proteins were shown on x -axis and log 10 signal intensity (combined for heavy and light peptides) on the y -axis. b Quantification of SDC4 and <t>DDX23</t> by 2-D HPLC LTQ/Orbitrap MS. Peaks with light-labeled (gray) and heavy-labeled (red) peptides were presented. VSMSSTVQGSNIFER and MIDMGFEPDVQKILEHMPVSNQK were peptides from SDC4 and DDX23, respectively. (R, Arginine; K, Lysine) m / z , mass/charge ratio. c Bufalin promoted the SDC4 binding to DDX23. Western blot of co-immunoprecipitation was performed with anti-SDC4 or anti-DDX23 antibodies. d Structure outline of SDC4 (upper panel). SDC4 interacts with DDX23 through its 1-170 amino acids peptide (lower panel). e Bufalin increased the number of γH2AX foci, which was blocked by siSDC4. Negative control or siSDC4 HepG2 cells were treated with/without bufalin, followed by γH2AX foci and DAPI staining. f , g siSDC4 or siDDX23 reversed bufalin-dependent cell viability decrease. Cells transfected with siSDC4, siDDX23 or negative control were treated with bufalin for 24 h. Cell viability was measured by MTT assay. h Cells transfected with siSDC4, siDDX23 or negative control were incubated with/without bufalin (10 nM) for 48 h. Wound area was calculated. Data are representative of three independent experiments. * P < 0.05, ** P < 0.01 vs . control group; ns, not significant by ANOVA with Student’s t -test.
    Antibodies Against Ddx23, supplied by Bioss, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against ddx23/product/Bioss
    Average 91 stars, based on 1 article reviews
    antibodies against ddx23 - by Bioz Stars, 2026-02
    91/100 stars

    Images

    1) Product Images from "Therapeutic potential of targeting membrane-spanning proteoglycan SDC4 in hepatocellular carcinoma"

    Article Title: Therapeutic potential of targeting membrane-spanning proteoglycan SDC4 in hepatocellular carcinoma

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-021-03780-y

    a Scatter plot depicted SDC4 interactome. Log 2 heavy (H) / light (L) ratios of the quantified proteins were shown on x -axis and log 10 signal intensity (combined for heavy and light peptides) on the y -axis. b Quantification of SDC4 and DDX23 by 2-D HPLC LTQ/Orbitrap MS. Peaks with light-labeled (gray) and heavy-labeled (red) peptides were presented. VSMSSTVQGSNIFER and MIDMGFEPDVQKILEHMPVSNQK were peptides from SDC4 and DDX23, respectively. (R, Arginine; K, Lysine) m / z , mass/charge ratio. c Bufalin promoted the SDC4 binding to DDX23. Western blot of co-immunoprecipitation was performed with anti-SDC4 or anti-DDX23 antibodies. d Structure outline of SDC4 (upper panel). SDC4 interacts with DDX23 through its 1-170 amino acids peptide (lower panel). e Bufalin increased the number of γH2AX foci, which was blocked by siSDC4. Negative control or siSDC4 HepG2 cells were treated with/without bufalin, followed by γH2AX foci and DAPI staining. f , g siSDC4 or siDDX23 reversed bufalin-dependent cell viability decrease. Cells transfected with siSDC4, siDDX23 or negative control were treated with bufalin for 24 h. Cell viability was measured by MTT assay. h Cells transfected with siSDC4, siDDX23 or negative control were incubated with/without bufalin (10 nM) for 48 h. Wound area was calculated. Data are representative of three independent experiments. * P < 0.05, ** P < 0.01 vs . control group; ns, not significant by ANOVA with Student’s t -test.
    Figure Legend Snippet: a Scatter plot depicted SDC4 interactome. Log 2 heavy (H) / light (L) ratios of the quantified proteins were shown on x -axis and log 10 signal intensity (combined for heavy and light peptides) on the y -axis. b Quantification of SDC4 and DDX23 by 2-D HPLC LTQ/Orbitrap MS. Peaks with light-labeled (gray) and heavy-labeled (red) peptides were presented. VSMSSTVQGSNIFER and MIDMGFEPDVQKILEHMPVSNQK were peptides from SDC4 and DDX23, respectively. (R, Arginine; K, Lysine) m / z , mass/charge ratio. c Bufalin promoted the SDC4 binding to DDX23. Western blot of co-immunoprecipitation was performed with anti-SDC4 or anti-DDX23 antibodies. d Structure outline of SDC4 (upper panel). SDC4 interacts with DDX23 through its 1-170 amino acids peptide (lower panel). e Bufalin increased the number of γH2AX foci, which was blocked by siSDC4. Negative control or siSDC4 HepG2 cells were treated with/without bufalin, followed by γH2AX foci and DAPI staining. f , g siSDC4 or siDDX23 reversed bufalin-dependent cell viability decrease. Cells transfected with siSDC4, siDDX23 or negative control were treated with bufalin for 24 h. Cell viability was measured by MTT assay. h Cells transfected with siSDC4, siDDX23 or negative control were incubated with/without bufalin (10 nM) for 48 h. Wound area was calculated. Data are representative of three independent experiments. * P < 0.05, ** P < 0.01 vs . control group; ns, not significant by ANOVA with Student’s t -test.

    Techniques Used: Labeling, Binding Assay, Western Blot, Immunoprecipitation, Negative Control, Staining, Transfection, MTT Assay, Incubation

    a , b siSDC4 blocked ERK/JNK/P38 MAPK, cell cycle, and MMP9 signaling pathways. CDK1, CyclinB1, P53, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were determined by western blot in SDC4 knockdown HepG2 cells. c , d siDDX23 prevented JNK/P38 MAPK, cell cycle, and MMP2/9 signaling pathways. CDK1, CyclinB1, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were detected by western blot in DDX23 knockdown HepG2 cells. e Correlation analysis between bufalin-regulated and siSDC4-altered proteins in HepG2 cells. f Correlation analysis between bufalin-regulated and siDDX23-altered proteins in HepG2 cells. Each data point represented the protein level (CDK1, CyclinB1, MMP2/9, and non-phosphorylations/phosphorylations of ERK/JNK/P38) changed by both bufalin and siSDC4 or siDDX23 treatment. Statistical significance was measured by Pearson’s correlation test. Data are expressed as mean ± SD for three individual experiments. ** P < 0.01 vs. control group; ns, not significant by ANOVA with Student’s t -test.
    Figure Legend Snippet: a , b siSDC4 blocked ERK/JNK/P38 MAPK, cell cycle, and MMP9 signaling pathways. CDK1, CyclinB1, P53, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were determined by western blot in SDC4 knockdown HepG2 cells. c , d siDDX23 prevented JNK/P38 MAPK, cell cycle, and MMP2/9 signaling pathways. CDK1, CyclinB1, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were detected by western blot in DDX23 knockdown HepG2 cells. e Correlation analysis between bufalin-regulated and siSDC4-altered proteins in HepG2 cells. f Correlation analysis between bufalin-regulated and siDDX23-altered proteins in HepG2 cells. Each data point represented the protein level (CDK1, CyclinB1, MMP2/9, and non-phosphorylations/phosphorylations of ERK/JNK/P38) changed by both bufalin and siSDC4 or siDDX23 treatment. Statistical significance was measured by Pearson’s correlation test. Data are expressed as mean ± SD for three individual experiments. ** P < 0.01 vs. control group; ns, not significant by ANOVA with Student’s t -test.

    Techniques Used: Western Blot



    Similar Products

    antibodies against ddx23  (Bioss)
    91
    Bioss antibodies against ddx23
    a Scatter plot depicted SDC4 interactome. Log 2 heavy (H) / light (L) ratios of the quantified proteins were shown on x -axis and log 10 signal intensity (combined for heavy and light peptides) on the y -axis. b Quantification of SDC4 and <t>DDX23</t> by 2-D HPLC LTQ/Orbitrap MS. Peaks with light-labeled (gray) and heavy-labeled (red) peptides were presented. VSMSSTVQGSNIFER and MIDMGFEPDVQKILEHMPVSNQK were peptides from SDC4 and DDX23, respectively. (R, Arginine; K, Lysine) m / z , mass/charge ratio. c Bufalin promoted the SDC4 binding to DDX23. Western blot of co-immunoprecipitation was performed with anti-SDC4 or anti-DDX23 antibodies. d Structure outline of SDC4 (upper panel). SDC4 interacts with DDX23 through its 1-170 amino acids peptide (lower panel). e Bufalin increased the number of γH2AX foci, which was blocked by siSDC4. Negative control or siSDC4 HepG2 cells were treated with/without bufalin, followed by γH2AX foci and DAPI staining. f , g siSDC4 or siDDX23 reversed bufalin-dependent cell viability decrease. Cells transfected with siSDC4, siDDX23 or negative control were treated with bufalin for 24 h. Cell viability was measured by MTT assay. h Cells transfected with siSDC4, siDDX23 or negative control were incubated with/without bufalin (10 nM) for 48 h. Wound area was calculated. Data are representative of three independent experiments. * P < 0.05, ** P < 0.01 vs . control group; ns, not significant by ANOVA with Student’s t -test.
    Antibodies Against Ddx23, supplied by Bioss, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against ddx23/product/Bioss
    Average 91 stars, based on 1 article reviews
    antibodies against ddx23 - by Bioz Stars, 2026-02
    91/100 stars
    		  Buy from Supplier

    Image Search Results


    a Scatter plot depicted SDC4 interactome. Log 2 heavy (H) / light (L) ratios of the quantified proteins were shown on x -axis and log 10 signal intensity (combined for heavy and light peptides) on the y -axis. b Quantification of SDC4 and DDX23 by 2-D HPLC LTQ/Orbitrap MS. Peaks with light-labeled (gray) and heavy-labeled (red) peptides were presented. VSMSSTVQGSNIFER and MIDMGFEPDVQKILEHMPVSNQK were peptides from SDC4 and DDX23, respectively. (R, Arginine; K, Lysine) m / z , mass/charge ratio. c Bufalin promoted the SDC4 binding to DDX23. Western blot of co-immunoprecipitation was performed with anti-SDC4 or anti-DDX23 antibodies. d Structure outline of SDC4 (upper panel). SDC4 interacts with DDX23 through its 1-170 amino acids peptide (lower panel). e Bufalin increased the number of γH2AX foci, which was blocked by siSDC4. Negative control or siSDC4 HepG2 cells were treated with/without bufalin, followed by γH2AX foci and DAPI staining. f , g siSDC4 or siDDX23 reversed bufalin-dependent cell viability decrease. Cells transfected with siSDC4, siDDX23 or negative control were treated with bufalin for 24 h. Cell viability was measured by MTT assay. h Cells transfected with siSDC4, siDDX23 or negative control were incubated with/without bufalin (10 nM) for 48 h. Wound area was calculated. Data are representative of three independent experiments. * P < 0.05, ** P < 0.01 vs . control group; ns, not significant by ANOVA with Student’s t -test.

    Journal: Cell Death & Disease

    Article Title: Therapeutic potential of targeting membrane-spanning proteoglycan SDC4 in hepatocellular carcinoma

    doi: 10.1038/s41419-021-03780-y

    Figure Lengend Snippet: a Scatter plot depicted SDC4 interactome. Log 2 heavy (H) / light (L) ratios of the quantified proteins were shown on x -axis and log 10 signal intensity (combined for heavy and light peptides) on the y -axis. b Quantification of SDC4 and DDX23 by 2-D HPLC LTQ/Orbitrap MS. Peaks with light-labeled (gray) and heavy-labeled (red) peptides were presented. VSMSSTVQGSNIFER and MIDMGFEPDVQKILEHMPVSNQK were peptides from SDC4 and DDX23, respectively. (R, Arginine; K, Lysine) m / z , mass/charge ratio. c Bufalin promoted the SDC4 binding to DDX23. Western blot of co-immunoprecipitation was performed with anti-SDC4 or anti-DDX23 antibodies. d Structure outline of SDC4 (upper panel). SDC4 interacts with DDX23 through its 1-170 amino acids peptide (lower panel). e Bufalin increased the number of γH2AX foci, which was blocked by siSDC4. Negative control or siSDC4 HepG2 cells were treated with/without bufalin, followed by γH2AX foci and DAPI staining. f , g siSDC4 or siDDX23 reversed bufalin-dependent cell viability decrease. Cells transfected with siSDC4, siDDX23 or negative control were treated with bufalin for 24 h. Cell viability was measured by MTT assay. h Cells transfected with siSDC4, siDDX23 or negative control were incubated with/without bufalin (10 nM) for 48 h. Wound area was calculated. Data are representative of three independent experiments. * P < 0.05, ** P < 0.01 vs . control group; ns, not significant by ANOVA with Student’s t -test.

    Article Snippet: Antibodies against DDX23 (bs-12199R) was from Bioss (Beijing, China).

    Techniques: Labeling, Binding Assay, Western Blot, Immunoprecipitation, Negative Control, Staining, Transfection, MTT Assay, Incubation

    a , b siSDC4 blocked ERK/JNK/P38 MAPK, cell cycle, and MMP9 signaling pathways. CDK1, CyclinB1, P53, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were determined by western blot in SDC4 knockdown HepG2 cells. c , d siDDX23 prevented JNK/P38 MAPK, cell cycle, and MMP2/9 signaling pathways. CDK1, CyclinB1, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were detected by western blot in DDX23 knockdown HepG2 cells. e Correlation analysis between bufalin-regulated and siSDC4-altered proteins in HepG2 cells. f Correlation analysis between bufalin-regulated and siDDX23-altered proteins in HepG2 cells. Each data point represented the protein level (CDK1, CyclinB1, MMP2/9, and non-phosphorylations/phosphorylations of ERK/JNK/P38) changed by both bufalin and siSDC4 or siDDX23 treatment. Statistical significance was measured by Pearson’s correlation test. Data are expressed as mean ± SD for three individual experiments. ** P < 0.01 vs. control group; ns, not significant by ANOVA with Student’s t -test.

    Journal: Cell Death & Disease

    Article Title: Therapeutic potential of targeting membrane-spanning proteoglycan SDC4 in hepatocellular carcinoma

    doi: 10.1038/s41419-021-03780-y

    Figure Lengend Snippet: a , b siSDC4 blocked ERK/JNK/P38 MAPK, cell cycle, and MMP9 signaling pathways. CDK1, CyclinB1, P53, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were determined by western blot in SDC4 knockdown HepG2 cells. c , d siDDX23 prevented JNK/P38 MAPK, cell cycle, and MMP2/9 signaling pathways. CDK1, CyclinB1, MMP2/9 and non-phosphorylations/phosphorylations of ERK/JNK/P38 were detected by western blot in DDX23 knockdown HepG2 cells. e Correlation analysis between bufalin-regulated and siSDC4-altered proteins in HepG2 cells. f Correlation analysis between bufalin-regulated and siDDX23-altered proteins in HepG2 cells. Each data point represented the protein level (CDK1, CyclinB1, MMP2/9, and non-phosphorylations/phosphorylations of ERK/JNK/P38) changed by both bufalin and siSDC4 or siDDX23 treatment. Statistical significance was measured by Pearson’s correlation test. Data are expressed as mean ± SD for three individual experiments. ** P < 0.01 vs. control group; ns, not significant by ANOVA with Student’s t -test.

    Article Snippet: Antibodies against DDX23 (bs-12199R) was from Bioss (Beijing, China).

    Techniques: Western Blot