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β actin antibody blocking peptide  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc β actin antibody blocking peptide
    miR-210 reduces DOX-induced apoptotic cell death in AC-16 cardiomyocytes. A Overexpressing miR-210 (OE) significantly attenuated caspase-3 activity, while ( B ) knocking down miR-210 (KD) significantly increased caspase-3 activity. Absorbance was measured at 405 nm. Caspase-3 activity was corrected for total protein content in each sample measured by β- Actin. All data are expressed as mean ± S.D. from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector
    β Actin Antibody Blocking Peptide, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/%CE%B2+actin+antibody+blocking+peptide/pmc12866067-9-0-12?v=Cell+Signaling+Technology+Inc
    Average 86 stars, based on 1 article reviews
    β actin antibody blocking peptide - by Bioz Stars, 2026-08
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    1) Product Images from "Cardiomyocyte overexpression of microRNA-210 mitigates apoptotic cell death induced by doxorubicin"

    Article Title: Cardiomyocyte overexpression of microRNA-210 mitigates apoptotic cell death induced by doxorubicin

    Journal: Cardio-oncology

    doi: 10.1186/s40959-025-00429-z

    miR-210 reduces DOX-induced apoptotic cell death in AC-16 cardiomyocytes. A Overexpressing miR-210 (OE) significantly attenuated caspase-3 activity, while ( B ) knocking down miR-210 (KD) significantly increased caspase-3 activity. Absorbance was measured at 405 nm. Caspase-3 activity was corrected for total protein content in each sample measured by β- Actin. All data are expressed as mean ± S.D. from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector
    Figure Legend Snippet: miR-210 reduces DOX-induced apoptotic cell death in AC-16 cardiomyocytes. A Overexpressing miR-210 (OE) significantly attenuated caspase-3 activity, while ( B ) knocking down miR-210 (KD) significantly increased caspase-3 activity. Absorbance was measured at 405 nm. Caspase-3 activity was corrected for total protein content in each sample measured by β- Actin. All data are expressed as mean ± S.D. from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector

    Techniques Used: Activity Assay, Over Expression, Knockdown, Standard Deviation, Plasmid Preparation

    miR-210 overexpression increases phosphorylation at serine 9 residue (Ser9) of glycogen synthase kinase-3β (GSK-3β)in DOX-treated AC-16 cardiomyocytes. A Phosphorylation at Ser9 of GSK-3β is increased with miR-210 OE vector as compared to EV after 24-h DOX treatment. B No significant difference in phosphorylation at Ser9 of GSK-3β is observed with miR-210 KD vector as compared to EV after 24-h DOX treatment. No change in protein expression levels of GSK-3βwere observed in AC-16 cardiomyocytes transfected with an overexpression (OE) vector ( C ) nor a knockdown (KD) vector ( D ) of miR-210 across all treatment arms. Protein expression of phosphorylation at Ser9 of GSK-3β was further confirmed by western blot under the condition of ( E ) miR-210 OE and ( F ) mir-210 KD. Protein expression of GSK-3β was corrected for total protein content in each sample measured by β- Actin. Absorbance was measured at 405 nm. All data are expressed as mean ± S.D. All data for ELISA analyses ( A - D ) was run from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. Panel G display exemplary western blot. Samples for was performed on three random selected samples from each group presented in panel A-D to allow comparison on the same gel.** p < 0.01; **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector
    Figure Legend Snippet: miR-210 overexpression increases phosphorylation at serine 9 residue (Ser9) of glycogen synthase kinase-3β (GSK-3β)in DOX-treated AC-16 cardiomyocytes. A Phosphorylation at Ser9 of GSK-3β is increased with miR-210 OE vector as compared to EV after 24-h DOX treatment. B No significant difference in phosphorylation at Ser9 of GSK-3β is observed with miR-210 KD vector as compared to EV after 24-h DOX treatment. No change in protein expression levels of GSK-3βwere observed in AC-16 cardiomyocytes transfected with an overexpression (OE) vector ( C ) nor a knockdown (KD) vector ( D ) of miR-210 across all treatment arms. Protein expression of phosphorylation at Ser9 of GSK-3β was further confirmed by western blot under the condition of ( E ) miR-210 OE and ( F ) mir-210 KD. Protein expression of GSK-3β was corrected for total protein content in each sample measured by β- Actin. Absorbance was measured at 405 nm. All data are expressed as mean ± S.D. All data for ELISA analyses ( A - D ) was run from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. Panel G display exemplary western blot. Samples for was performed on three random selected samples from each group presented in panel A-D to allow comparison on the same gel.** p < 0.01; **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector

    Techniques Used: Over Expression, Phospho-proteomics, Residue, Plasmid Preparation, Expressing, Transfection, Knockdown, Western Blot, Enzyme-linked Immunosorbent Assay, Comparison, Standard Deviation

    miR-210 affects phosphorylation of Akt at serine 473 (Ser473) in DOX-treated AC-16 cardiomyocytes. No change in protein expression levels of Akt were observed in AC-16 cardiomyocytes transfected with either ( A ) the overexpression (OE) vector of miR-210 or the knock down vector (KD) ( B ). C Phosphorylation at Ser473 of Akt is increased with miR-210 OE vector as compared to EV after 24-h DOX treatment. D A significantly lower degree of phosphorylation at Ser473 of Akt is observed with miR-210 KD vector as compared to empty vector (EV) after 24-h DOX treatment. All data for ELISA analyses was run from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. Expression levels of phosphorylation at Ser473 of Akt was further confirmed by western blot under the condition of ( E ) the overexpression miR-210 OE and ( F ) mir-210 KD. Absorbance was measured at 405 nm. Protein expression of Akt was corrected for total protein content in each sample measured by β- Actin that also served as control for expression of GSK-3β protein loading. Panel G display exemplary western blot. Samples for was performed on three random selected samples from each group presented in panel A-D to allow comparison on the same gel. * p < 0.05; ** p < 0.01; **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. -/+ to each group for DOX denotes if the condition of the cells were with DOX (+) or with vehicle treatment (-). For miR-210 OE -/+ denotes if cells where treated by miR-210 OE (+) or denotes the treatment were EV (-). For miR-210 KD -/+ denotes if cells were treated by miR-210 KD (+) or denotes the treatment were EV (-)
    Figure Legend Snippet: miR-210 affects phosphorylation of Akt at serine 473 (Ser473) in DOX-treated AC-16 cardiomyocytes. No change in protein expression levels of Akt were observed in AC-16 cardiomyocytes transfected with either ( A ) the overexpression (OE) vector of miR-210 or the knock down vector (KD) ( B ). C Phosphorylation at Ser473 of Akt is increased with miR-210 OE vector as compared to EV after 24-h DOX treatment. D A significantly lower degree of phosphorylation at Ser473 of Akt is observed with miR-210 KD vector as compared to empty vector (EV) after 24-h DOX treatment. All data for ELISA analyses was run from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. Expression levels of phosphorylation at Ser473 of Akt was further confirmed by western blot under the condition of ( E ) the overexpression miR-210 OE and ( F ) mir-210 KD. Absorbance was measured at 405 nm. Protein expression of Akt was corrected for total protein content in each sample measured by β- Actin that also served as control for expression of GSK-3β protein loading. Panel G display exemplary western blot. Samples for was performed on three random selected samples from each group presented in panel A-D to allow comparison on the same gel. * p < 0.05; ** p < 0.01; **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. -/+ to each group for DOX denotes if the condition of the cells were with DOX (+) or with vehicle treatment (-). For miR-210 OE -/+ denotes if cells where treated by miR-210 OE (+) or denotes the treatment were EV (-). For miR-210 KD -/+ denotes if cells were treated by miR-210 KD (+) or denotes the treatment were EV (-)

    Techniques Used: Phospho-proteomics, Expressing, Transfection, Over Expression, Plasmid Preparation, Knockdown, Enzyme-linked Immunosorbent Assay, Western Blot, Control, Comparison, Standard Deviation, IF-cells



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    Cell Signaling Technology Inc β actin antibody blocking peptide
    miR-210 reduces DOX-induced apoptotic cell death in AC-16 cardiomyocytes. A Overexpressing miR-210 (OE) significantly attenuated caspase-3 activity, while ( B ) knocking down miR-210 (KD) significantly increased caspase-3 activity. Absorbance was measured at 405 nm. Caspase-3 activity was corrected for total protein content in each sample measured by β- Actin. All data are expressed as mean ± S.D. from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector
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    miR-210 reduces DOX-induced apoptotic cell death in AC-16 cardiomyocytes. A Overexpressing miR-210 (OE) significantly attenuated caspase-3 activity, while ( B ) knocking down miR-210 (KD) significantly increased caspase-3 activity. Absorbance was measured at 405 nm. Caspase-3 activity was corrected for total protein content in each sample measured by β- Actin. All data are expressed as mean ± S.D. from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector

    Journal: Cardio-oncology

    Article Title: Cardiomyocyte overexpression of microRNA-210 mitigates apoptotic cell death induced by doxorubicin

    doi: 10.1186/s40959-025-00429-z

    Figure Lengend Snippet: miR-210 reduces DOX-induced apoptotic cell death in AC-16 cardiomyocytes. A Overexpressing miR-210 (OE) significantly attenuated caspase-3 activity, while ( B ) knocking down miR-210 (KD) significantly increased caspase-3 activity. Absorbance was measured at 405 nm. Caspase-3 activity was corrected for total protein content in each sample measured by β- Actin. All data are expressed as mean ± S.D. from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector

    Article Snippet: β-Actin antibody blocking peptide , ELISA detection , N/A , N/A , Cell Signalling Technology , 1025.

    Techniques: Activity Assay, Over Expression, Knockdown, Standard Deviation, Plasmid Preparation

    miR-210 overexpression increases phosphorylation at serine 9 residue (Ser9) of glycogen synthase kinase-3β (GSK-3β)in DOX-treated AC-16 cardiomyocytes. A Phosphorylation at Ser9 of GSK-3β is increased with miR-210 OE vector as compared to EV after 24-h DOX treatment. B No significant difference in phosphorylation at Ser9 of GSK-3β is observed with miR-210 KD vector as compared to EV after 24-h DOX treatment. No change in protein expression levels of GSK-3βwere observed in AC-16 cardiomyocytes transfected with an overexpression (OE) vector ( C ) nor a knockdown (KD) vector ( D ) of miR-210 across all treatment arms. Protein expression of phosphorylation at Ser9 of GSK-3β was further confirmed by western blot under the condition of ( E ) miR-210 OE and ( F ) mir-210 KD. Protein expression of GSK-3β was corrected for total protein content in each sample measured by β- Actin. Absorbance was measured at 405 nm. All data are expressed as mean ± S.D. All data for ELISA analyses ( A - D ) was run from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. Panel G display exemplary western blot. Samples for was performed on three random selected samples from each group presented in panel A-D to allow comparison on the same gel.** p < 0.01; **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector

    Journal: Cardio-oncology

    Article Title: Cardiomyocyte overexpression of microRNA-210 mitigates apoptotic cell death induced by doxorubicin

    doi: 10.1186/s40959-025-00429-z

    Figure Lengend Snippet: miR-210 overexpression increases phosphorylation at serine 9 residue (Ser9) of glycogen synthase kinase-3β (GSK-3β)in DOX-treated AC-16 cardiomyocytes. A Phosphorylation at Ser9 of GSK-3β is increased with miR-210 OE vector as compared to EV after 24-h DOX treatment. B No significant difference in phosphorylation at Ser9 of GSK-3β is observed with miR-210 KD vector as compared to EV after 24-h DOX treatment. No change in protein expression levels of GSK-3βwere observed in AC-16 cardiomyocytes transfected with an overexpression (OE) vector ( C ) nor a knockdown (KD) vector ( D ) of miR-210 across all treatment arms. Protein expression of phosphorylation at Ser9 of GSK-3β was further confirmed by western blot under the condition of ( E ) miR-210 OE and ( F ) mir-210 KD. Protein expression of GSK-3β was corrected for total protein content in each sample measured by β- Actin. Absorbance was measured at 405 nm. All data are expressed as mean ± S.D. All data for ELISA analyses ( A - D ) was run from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. Panel G display exemplary western blot. Samples for was performed on three random selected samples from each group presented in panel A-D to allow comparison on the same gel.** p < 0.01; **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. Notation: “ + ” indicates treatment applied; “–” indicates absence of treatment. For DOX, “ + ” = DOX-treated, “–” = vehicle. For miR-210 OE, “ + ” = miR-210 OE, “–” = empty vector. For miR-210 KD, “ + ” = miR-210 knockdown, “–” = empty vector

    Article Snippet: β-Actin antibody blocking peptide , ELISA detection , N/A , N/A , Cell Signalling Technology , 1025.

    Techniques: Over Expression, Phospho-proteomics, Residue, Plasmid Preparation, Expressing, Transfection, Knockdown, Western Blot, Enzyme-linked Immunosorbent Assay, Comparison, Standard Deviation

    miR-210 affects phosphorylation of Akt at serine 473 (Ser473) in DOX-treated AC-16 cardiomyocytes. No change in protein expression levels of Akt were observed in AC-16 cardiomyocytes transfected with either ( A ) the overexpression (OE) vector of miR-210 or the knock down vector (KD) ( B ). C Phosphorylation at Ser473 of Akt is increased with miR-210 OE vector as compared to EV after 24-h DOX treatment. D A significantly lower degree of phosphorylation at Ser473 of Akt is observed with miR-210 KD vector as compared to empty vector (EV) after 24-h DOX treatment. All data for ELISA analyses was run from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. Expression levels of phosphorylation at Ser473 of Akt was further confirmed by western blot under the condition of ( E ) the overexpression miR-210 OE and ( F ) mir-210 KD. Absorbance was measured at 405 nm. Protein expression of Akt was corrected for total protein content in each sample measured by β- Actin that also served as control for expression of GSK-3β protein loading. Panel G display exemplary western blot. Samples for was performed on three random selected samples from each group presented in panel A-D to allow comparison on the same gel. * p < 0.05; ** p < 0.01; **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. -/+ to each group for DOX denotes if the condition of the cells were with DOX (+) or with vehicle treatment (-). For miR-210 OE -/+ denotes if cells where treated by miR-210 OE (+) or denotes the treatment were EV (-). For miR-210 KD -/+ denotes if cells were treated by miR-210 KD (+) or denotes the treatment were EV (-)

    Journal: Cardio-oncology

    Article Title: Cardiomyocyte overexpression of microRNA-210 mitigates apoptotic cell death induced by doxorubicin

    doi: 10.1186/s40959-025-00429-z

    Figure Lengend Snippet: miR-210 affects phosphorylation of Akt at serine 473 (Ser473) in DOX-treated AC-16 cardiomyocytes. No change in protein expression levels of Akt were observed in AC-16 cardiomyocytes transfected with either ( A ) the overexpression (OE) vector of miR-210 or the knock down vector (KD) ( B ). C Phosphorylation at Ser473 of Akt is increased with miR-210 OE vector as compared to EV after 24-h DOX treatment. D A significantly lower degree of phosphorylation at Ser473 of Akt is observed with miR-210 KD vector as compared to empty vector (EV) after 24-h DOX treatment. All data for ELISA analyses was run from three technical replicates for each of the four biological replicates ( n = 4) belonging to each experimental group. Expression levels of phosphorylation at Ser473 of Akt was further confirmed by western blot under the condition of ( E ) the overexpression miR-210 OE and ( F ) mir-210 KD. Absorbance was measured at 405 nm. Protein expression of Akt was corrected for total protein content in each sample measured by β- Actin that also served as control for expression of GSK-3β protein loading. Panel G display exemplary western blot. Samples for was performed on three random selected samples from each group presented in panel A-D to allow comparison on the same gel. * p < 0.05; ** p < 0.01; **** p < 0.0001. DOX: doxorubicin; OE: miR-210 overexpression; KD: miR-210 knockdown; S.D.: standard deviation. -/+ to each group for DOX denotes if the condition of the cells were with DOX (+) or with vehicle treatment (-). For miR-210 OE -/+ denotes if cells where treated by miR-210 OE (+) or denotes the treatment were EV (-). For miR-210 KD -/+ denotes if cells were treated by miR-210 KD (+) or denotes the treatment were EV (-)

    Article Snippet: β-Actin antibody blocking peptide , ELISA detection , N/A , N/A , Cell Signalling Technology , 1025.

    Techniques: Phospho-proteomics, Expressing, Transfection, Over Expression, Plasmid Preparation, Knockdown, Enzyme-linked Immunosorbent Assay, Western Blot, Control, Comparison, Standard Deviation, IF-cells

    List of antibodies and antibody-blocking peptides used in the study.

    Journal: International Journal of Molecular Sciences

    Article Title: NF-κB Transcriptional Activity Indispensably Mediates Hypoxia–Reoxygenation Stress-Induced microRNA-210 Expression

    doi: 10.3390/ijms24076618

    Figure Lengend Snippet: List of antibodies and antibody-blocking peptides used in the study.

    Article Snippet: β-Actin Antibody-Blocking Peptide , ELISA detection , N/A , N/A , Cell Signaling Technology, Danvers, MA, USA , 1025.

    Techniques: Enzyme-linked Immunosorbent Assay, Peptide ELISA