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Santa Cruz Biotechnology j 414 hnrnpa2b1
J 414 Hnrnpa2b1, supplied by Santa Cruz Biotechnology, 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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j 414 hnrnpa2b1 - by Bioz Stars, 2024-07
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bsa cst 3181 elk 1 rabbit  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc bsa cst 3181 elk 1 rabbit
    List of Primary Antibodies Used in the Study
    Bsa Cst 3181 Elk 1 Rabbit, 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/bsa cst 3181 elk 1 rabbit/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bsa cst 3181 elk 1 rabbit - by Bioz Stars, 2024-07
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    1) Product Images from "Platelet-Derived Growth Factor Receptor α Contributes to Human Hepatic Stellate Cell Proliferation and Migration"

    Article Title: Platelet-Derived Growth Factor Receptor α Contributes to Human Hepatic Stellate Cell Proliferation and Migration

    Journal: The American Journal of Pathology

    doi: 10.1016/j.ajpath.2017.06.009

    List of Primary Antibodies Used in the Study
    Figure Legend Snippet: List of Primary Antibodies Used in the Study

    Techniques Used: Blocking Assay

    Olaratumab inhibits PDGFRα activation and downstream proliferative signaling mediators in HHSteCs in the presence of exogenous PDGF stimulation. A and B: HHSteCs were pretreated with either 300 nmol/L olaratumab or 300 nmol/L human IgG for 30 minutes (m) before 10 ng/mL PDGF-BB exposure for the indicated time periods. Representative Western blots using pooled samples from each time point from three technical replicates show decrease in phosphorylation of tyrosine residues in PDGFRα in cells pretreated with olaratumab, including Y754, Y762, Y849, and Y1018, but not Y742 and Y572/574. Arrowheads indicate the correct molecular weight band. C and D: Representative Western blots using pooled samples from each time point from three technical replicates also show decreased phosphorylation of p38 MAPK (T180/Y182), FAK (Y397, Y576/Y577, Y925), Akt (Ser473), and mTOR (Ser2448, Ser2481) after PDGFRα blockade with 300 nmol/L olaratumab before 10 ng/mL PDGF-BB treatment. E: Decreased phosphorylation of Erk1/2 (T202/Y204) and downstream transcription factor Elk1 (Ser383) was also observed in similar representative Western blots. Ponceau staining is included as a loading control. All Western blots were repeated twice on the same pooled lysates from three technical replicates and performed for the two stellate cell batches. h, hour; NT, nontreated.
    Figure Legend Snippet: Olaratumab inhibits PDGFRα activation and downstream proliferative signaling mediators in HHSteCs in the presence of exogenous PDGF stimulation. A and B: HHSteCs were pretreated with either 300 nmol/L olaratumab or 300 nmol/L human IgG for 30 minutes (m) before 10 ng/mL PDGF-BB exposure for the indicated time periods. Representative Western blots using pooled samples from each time point from three technical replicates show decrease in phosphorylation of tyrosine residues in PDGFRα in cells pretreated with olaratumab, including Y754, Y762, Y849, and Y1018, but not Y742 and Y572/574. Arrowheads indicate the correct molecular weight band. C and D: Representative Western blots using pooled samples from each time point from three technical replicates also show decreased phosphorylation of p38 MAPK (T180/Y182), FAK (Y397, Y576/Y577, Y925), Akt (Ser473), and mTOR (Ser2448, Ser2481) after PDGFRα blockade with 300 nmol/L olaratumab before 10 ng/mL PDGF-BB treatment. E: Decreased phosphorylation of Erk1/2 (T202/Y204) and downstream transcription factor Elk1 (Ser383) was also observed in similar representative Western blots. Ponceau staining is included as a loading control. All Western blots were repeated twice on the same pooled lysates from three technical replicates and performed for the two stellate cell batches. h, hour; NT, nontreated.

    Techniques Used: Activation Assay, Western Blot, Molecular Weight, Staining

    Olaratumab inhibits baseline PDGFRα signaling in HHSteCs along with downstream effectors. A: Representative Western blots from HHSteC treatment with 300 nmol/L olaratumab using pooled lysates from three technical replicates for each time point showing decreased PDGFRα phosphorylation at Y762 and Y849 compared to IgG-treated controls. PDGF-BB treatment included as a positive control. B: Similar representative Western blots showing decreased Erk and Elk-1 phosphorylation compared to IgG-treated controls. PDGF-BB treatment serves as a positive control. C: Representative Western blots show olaratumab treatment decreases phosphorylation of mTOR at Ser2448 and increases phosphorylation at Ser2481. Olaratumab also decreases p38 phosphorylation. D: Similar representative Western blots showing olaratumab treatment increasing Abl expression and phosphorylation at Y412 and Y89 and increasing phosphorylation at inhibitory tyrosine residues of CrkII (Y221) and CrkL (Y207). Arrowhead indicates the correct molecular weight band. E: Immunoprecipitation of HHSteC lysates using anti-CrkII shows increased binding of CrkII to both total PDGFRα and phospho-PDGFRα Y762 after olaratumab treatment. Ponceau staining is included as a loading control. All Western blots were repeated twice on the same pooled lysates from three technical replicates and performed for the two stellate cell batches. h, hours; IP, immunoprecipitation; m, minutes; WB, Western blotting.
    Figure Legend Snippet: Olaratumab inhibits baseline PDGFRα signaling in HHSteCs along with downstream effectors. A: Representative Western blots from HHSteC treatment with 300 nmol/L olaratumab using pooled lysates from three technical replicates for each time point showing decreased PDGFRα phosphorylation at Y762 and Y849 compared to IgG-treated controls. PDGF-BB treatment included as a positive control. B: Similar representative Western blots showing decreased Erk and Elk-1 phosphorylation compared to IgG-treated controls. PDGF-BB treatment serves as a positive control. C: Representative Western blots show olaratumab treatment decreases phosphorylation of mTOR at Ser2448 and increases phosphorylation at Ser2481. Olaratumab also decreases p38 phosphorylation. D: Similar representative Western blots showing olaratumab treatment increasing Abl expression and phosphorylation at Y412 and Y89 and increasing phosphorylation at inhibitory tyrosine residues of CrkII (Y221) and CrkL (Y207). Arrowhead indicates the correct molecular weight band. E: Immunoprecipitation of HHSteC lysates using anti-CrkII shows increased binding of CrkII to both total PDGFRα and phospho-PDGFRα Y762 after olaratumab treatment. Ponceau staining is included as a loading control. All Western blots were repeated twice on the same pooled lysates from three technical replicates and performed for the two stellate cell batches. h, hours; IP, immunoprecipitation; m, minutes; WB, Western blotting.

    Techniques Used: Western Blot, Positive Control, Expressing, Molecular Weight, Immunoprecipitation, Binding Assay, Staining

    Proposed effect of PDGFRα blockade on HSC migration and proliferation through inhibition of specific downstream signaling. A: In response to PDGFRα activation by autocrine and/or exogenous PDGF, HSC proliferation and migration are induced through activation of FAK, Erk1/2, Elk-1, p38, Akt, mTOR, and CrkII/CrkL signaling. B: Blockade of PDGFRα by olaratumab decreases the above-mentioned signaling mediators, with FAK, Erk1/2, Elk-1, mTOR, and Akt affecting proliferation and Erk1/2, Elk-1, p38, CrkII/CrkL, decreased mTORC1, and increased mTORC2 regulating migration. Decreases in downstream signaling are represented by dashed arrows.
    Figure Legend Snippet: Proposed effect of PDGFRα blockade on HSC migration and proliferation through inhibition of specific downstream signaling. A: In response to PDGFRα activation by autocrine and/or exogenous PDGF, HSC proliferation and migration are induced through activation of FAK, Erk1/2, Elk-1, p38, Akt, mTOR, and CrkII/CrkL signaling. B: Blockade of PDGFRα by olaratumab decreases the above-mentioned signaling mediators, with FAK, Erk1/2, Elk-1, mTOR, and Akt affecting proliferation and Erk1/2, Elk-1, p38, CrkII/CrkL, decreased mTORC1, and increased mTORC2 regulating migration. Decreases in downstream signaling are represented by dashed arrows.

    Techniques Used: Migration, Inhibition, Activation Assay

    bsa cst 3181 elk 1 rabbit  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc bsa cst 3181 elk 1 rabbit
    List of Primary Antibodies Used in the Study
    Bsa Cst 3181 Elk 1 Rabbit, 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/bsa cst 3181 elk 1 rabbit/product/Cell Signaling Technology Inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bsa cst 3181 elk 1 rabbit - by Bioz Stars, 2024-07
    95/100 stars

    Images

    1) Product Images from "Platelet-Derived Growth Factor Receptor α Contributes to Human Hepatic Stellate Cell Proliferation and Migration"

    Article Title: Platelet-Derived Growth Factor Receptor α Contributes to Human Hepatic Stellate Cell Proliferation and Migration

    Journal: The American Journal of Pathology

    doi: 10.1016/j.ajpath.2017.06.009

    List of Primary Antibodies Used in the Study
    Figure Legend Snippet: List of Primary Antibodies Used in the Study

    Techniques Used: Blocking Assay

    Olaratumab inhibits PDGFRα activation and downstream proliferative signaling mediators in HHSteCs in the presence of exogenous PDGF stimulation. A and B: HHSteCs were pretreated with either 300 nmol/L olaratumab or 300 nmol/L human IgG for 30 minutes (m) before 10 ng/mL PDGF-BB exposure for the indicated time periods. Representative Western blots using pooled samples from each time point from three technical replicates show decrease in phosphorylation of tyrosine residues in PDGFRα in cells pretreated with olaratumab, including Y754, Y762, Y849, and Y1018, but not Y742 and Y572/574. Arrowheads indicate the correct molecular weight band. C and D: Representative Western blots using pooled samples from each time point from three technical replicates also show decreased phosphorylation of p38 MAPK (T180/Y182), FAK (Y397, Y576/Y577, Y925), Akt (Ser473), and mTOR (Ser2448, Ser2481) after PDGFRα blockade with 300 nmol/L olaratumab before 10 ng/mL PDGF-BB treatment. E: Decreased phosphorylation of Erk1/2 (T202/Y204) and downstream transcription factor Elk1 (Ser383) was also observed in similar representative Western blots. Ponceau staining is included as a loading control. All Western blots were repeated twice on the same pooled lysates from three technical replicates and performed for the two stellate cell batches. h, hour; NT, nontreated.
    Figure Legend Snippet: Olaratumab inhibits PDGFRα activation and downstream proliferative signaling mediators in HHSteCs in the presence of exogenous PDGF stimulation. A and B: HHSteCs were pretreated with either 300 nmol/L olaratumab or 300 nmol/L human IgG for 30 minutes (m) before 10 ng/mL PDGF-BB exposure for the indicated time periods. Representative Western blots using pooled samples from each time point from three technical replicates show decrease in phosphorylation of tyrosine residues in PDGFRα in cells pretreated with olaratumab, including Y754, Y762, Y849, and Y1018, but not Y742 and Y572/574. Arrowheads indicate the correct molecular weight band. C and D: Representative Western blots using pooled samples from each time point from three technical replicates also show decreased phosphorylation of p38 MAPK (T180/Y182), FAK (Y397, Y576/Y577, Y925), Akt (Ser473), and mTOR (Ser2448, Ser2481) after PDGFRα blockade with 300 nmol/L olaratumab before 10 ng/mL PDGF-BB treatment. E: Decreased phosphorylation of Erk1/2 (T202/Y204) and downstream transcription factor Elk1 (Ser383) was also observed in similar representative Western blots. Ponceau staining is included as a loading control. All Western blots were repeated twice on the same pooled lysates from three technical replicates and performed for the two stellate cell batches. h, hour; NT, nontreated.

    Techniques Used: Activation Assay, Western Blot, Molecular Weight, Staining

    Olaratumab inhibits baseline PDGFRα signaling in HHSteCs along with downstream effectors. A: Representative Western blots from HHSteC treatment with 300 nmol/L olaratumab using pooled lysates from three technical replicates for each time point showing decreased PDGFRα phosphorylation at Y762 and Y849 compared to IgG-treated controls. PDGF-BB treatment included as a positive control. B: Similar representative Western blots showing decreased Erk and Elk-1 phosphorylation compared to IgG-treated controls. PDGF-BB treatment serves as a positive control. C: Representative Western blots show olaratumab treatment decreases phosphorylation of mTOR at Ser2448 and increases phosphorylation at Ser2481. Olaratumab also decreases p38 phosphorylation. D: Similar representative Western blots showing olaratumab treatment increasing Abl expression and phosphorylation at Y412 and Y89 and increasing phosphorylation at inhibitory tyrosine residues of CrkII (Y221) and CrkL (Y207). Arrowhead indicates the correct molecular weight band. E: Immunoprecipitation of HHSteC lysates using anti-CrkII shows increased binding of CrkII to both total PDGFRα and phospho-PDGFRα Y762 after olaratumab treatment. Ponceau staining is included as a loading control. All Western blots were repeated twice on the same pooled lysates from three technical replicates and performed for the two stellate cell batches. h, hours; IP, immunoprecipitation; m, minutes; WB, Western blotting.
    Figure Legend Snippet: Olaratumab inhibits baseline PDGFRα signaling in HHSteCs along with downstream effectors. A: Representative Western blots from HHSteC treatment with 300 nmol/L olaratumab using pooled lysates from three technical replicates for each time point showing decreased PDGFRα phosphorylation at Y762 and Y849 compared to IgG-treated controls. PDGF-BB treatment included as a positive control. B: Similar representative Western blots showing decreased Erk and Elk-1 phosphorylation compared to IgG-treated controls. PDGF-BB treatment serves as a positive control. C: Representative Western blots show olaratumab treatment decreases phosphorylation of mTOR at Ser2448 and increases phosphorylation at Ser2481. Olaratumab also decreases p38 phosphorylation. D: Similar representative Western blots showing olaratumab treatment increasing Abl expression and phosphorylation at Y412 and Y89 and increasing phosphorylation at inhibitory tyrosine residues of CrkII (Y221) and CrkL (Y207). Arrowhead indicates the correct molecular weight band. E: Immunoprecipitation of HHSteC lysates using anti-CrkII shows increased binding of CrkII to both total PDGFRα and phospho-PDGFRα Y762 after olaratumab treatment. Ponceau staining is included as a loading control. All Western blots were repeated twice on the same pooled lysates from three technical replicates and performed for the two stellate cell batches. h, hours; IP, immunoprecipitation; m, minutes; WB, Western blotting.

    Techniques Used: Western Blot, Positive Control, Expressing, Molecular Weight, Immunoprecipitation, Binding Assay, Staining

    Proposed effect of PDGFRα blockade on HSC migration and proliferation through inhibition of specific downstream signaling. A: In response to PDGFRα activation by autocrine and/or exogenous PDGF, HSC proliferation and migration are induced through activation of FAK, Erk1/2, Elk-1, p38, Akt, mTOR, and CrkII/CrkL signaling. B: Blockade of PDGFRα by olaratumab decreases the above-mentioned signaling mediators, with FAK, Erk1/2, Elk-1, mTOR, and Akt affecting proliferation and Erk1/2, Elk-1, p38, CrkII/CrkL, decreased mTORC1, and increased mTORC2 regulating migration. Decreases in downstream signaling are represented by dashed arrows.
    Figure Legend Snippet: Proposed effect of PDGFRα blockade on HSC migration and proliferation through inhibition of specific downstream signaling. A: In response to PDGFRα activation by autocrine and/or exogenous PDGF, HSC proliferation and migration are induced through activation of FAK, Erk1/2, Elk-1, p38, Akt, mTOR, and CrkII/CrkL signaling. B: Blockade of PDGFRα by olaratumab decreases the above-mentioned signaling mediators, with FAK, Erk1/2, Elk-1, mTOR, and Akt affecting proliferation and Erk1/2, Elk-1, p38, CrkII/CrkL, decreased mTORC1, and increased mTORC2 regulating migration. Decreases in downstream signaling are represented by dashed arrows.

    Techniques Used: Migration, Inhibition, Activation Assay

    l affaire hoffman v monsanto canada 3181 droit vol 52 2 juin 11  (Monsanto Company)

     
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    Monsanto Company l affaire hoffman v monsanto canada 3181 droit vol 52 2 juin 11
    L Affaire Hoffman V Monsanto Canada 3181 Droit Vol 52 2 Juin 11, supplied by Monsanto Company, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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