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anti human poly adp ribose polymerase  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti human poly adp ribose polymerase
    Myrrh reduces the growth of human endometriotic cells by activating apoptotic signaling pathways. Endometriotic cells (12Z) and normal endometrial cells (T-HESC) were treated with the indicated concentrations of myrrh. (A) Cell viability was analyzed by measuring at 450 nm wavelength using MTT after 24 h. (B) To assess apoptotic or dead cell populations, 12Z cells were treated with increasing doses of myrrh for 24 h, and the percentages of Annexin V-positive and PI-positive cells were measured (Annexin V: Ex 494/Em 525 nm; PI: Ex 535/Em 617 nm). After 24 h of treatment with each concentration of myrrh, mitochondria-associated apoptotic proteins were analyzed by immunoblotting. (C) Representatives immunoblot images of Bax and Bcl-2 are shown. (D) A major monomeric Bax band at ~21 kDa (monomer Bax) and higher-molecular-weight bands corresponding to oligomeric forms (tetramer Bax, ~84 kDa) are indicated. (E) Representative immunoblot images of caspase-3, caspase-9 and PARP are shown. GAPDH was used as an internal control. (F) Densitometric analysis of protein levels. Data are expressed as relative intensity compared to control. Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. * P<0.05, ** P<0.01 and *** P<0.001. Ex, excitation; Em, emission; ; PARP, <t>poly(ADP-ribose)</t> <t>polymerase.</t>
    Anti Human Poly Adp Ribose Polymerase, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 15014 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/poly+adp+ribose+polymerases/pmc12902740-93-15-21?v=Cell+Signaling+Technology+Inc
    Average 98 stars, based on 15014 article reviews
    anti human poly adp ribose polymerase - by Bioz Stars, 2026-07
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    1) Product Images from "Myrrh ameliorates endometriosis by enhancing ER stress-related apoptotic cell death"

    Article Title: Myrrh ameliorates endometriosis by enhancing ER stress-related apoptotic cell death

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2026.13080

    Myrrh reduces the growth of human endometriotic cells by activating apoptotic signaling pathways. Endometriotic cells (12Z) and normal endometrial cells (T-HESC) were treated with the indicated concentrations of myrrh. (A) Cell viability was analyzed by measuring at 450 nm wavelength using MTT after 24 h. (B) To assess apoptotic or dead cell populations, 12Z cells were treated with increasing doses of myrrh for 24 h, and the percentages of Annexin V-positive and PI-positive cells were measured (Annexin V: Ex 494/Em 525 nm; PI: Ex 535/Em 617 nm). After 24 h of treatment with each concentration of myrrh, mitochondria-associated apoptotic proteins were analyzed by immunoblotting. (C) Representatives immunoblot images of Bax and Bcl-2 are shown. (D) A major monomeric Bax band at ~21 kDa (monomer Bax) and higher-molecular-weight bands corresponding to oligomeric forms (tetramer Bax, ~84 kDa) are indicated. (E) Representative immunoblot images of caspase-3, caspase-9 and PARP are shown. GAPDH was used as an internal control. (F) Densitometric analysis of protein levels. Data are expressed as relative intensity compared to control. Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. * P<0.05, ** P<0.01 and *** P<0.001. Ex, excitation; Em, emission; ; PARP, poly(ADP-ribose) polymerase.
    Figure Legend Snippet: Myrrh reduces the growth of human endometriotic cells by activating apoptotic signaling pathways. Endometriotic cells (12Z) and normal endometrial cells (T-HESC) were treated with the indicated concentrations of myrrh. (A) Cell viability was analyzed by measuring at 450 nm wavelength using MTT after 24 h. (B) To assess apoptotic or dead cell populations, 12Z cells were treated with increasing doses of myrrh for 24 h, and the percentages of Annexin V-positive and PI-positive cells were measured (Annexin V: Ex 494/Em 525 nm; PI: Ex 535/Em 617 nm). After 24 h of treatment with each concentration of myrrh, mitochondria-associated apoptotic proteins were analyzed by immunoblotting. (C) Representatives immunoblot images of Bax and Bcl-2 are shown. (D) A major monomeric Bax band at ~21 kDa (monomer Bax) and higher-molecular-weight bands corresponding to oligomeric forms (tetramer Bax, ~84 kDa) are indicated. (E) Representative immunoblot images of caspase-3, caspase-9 and PARP are shown. GAPDH was used as an internal control. (F) Densitometric analysis of protein levels. Data are expressed as relative intensity compared to control. Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. * P<0.05, ** P<0.01 and *** P<0.001. Ex, excitation; Em, emission; ; PARP, poly(ADP-ribose) polymerase.

    Techniques Used: Protein-Protein interactions, Concentration Assay, Western Blot, Molecular Weight, Control

    Mechanism of action of myrrh in endometriosis. (A) 12Z were treated with the indicated concentrations of myrrh and TUDCA (200 µM). Cell viability was analyzed using MTT after 24 h, measured at a wavelength of 450 nm. (B) Schematic representation summarizing the experimental results and the potential mechanism by which myrrh exerts palliative effects on endometriosis. *** P<0.001. TUDCA, tauroursodeoxycholic acid; ATF6, activating transcription factor 6; IRE1α, inositol-requiring enzyme 1 alpha; ATF4, activating transcription factor 4; CHOP, C/EBP homologous protein; GADD34, growth arrest and DNA damage-inducible protein 34; Bax, Bcl-2-associated X protein; Bcl2, B-cell lymphoma 2; Caspase 3, cysteine-aspartic acid protease 3; Caspase 9, cysteine-aspartic acid protease 9; PARP, poly(ADP-ribose) polymerase.
    Figure Legend Snippet: Mechanism of action of myrrh in endometriosis. (A) 12Z were treated with the indicated concentrations of myrrh and TUDCA (200 µM). Cell viability was analyzed using MTT after 24 h, measured at a wavelength of 450 nm. (B) Schematic representation summarizing the experimental results and the potential mechanism by which myrrh exerts palliative effects on endometriosis. *** P<0.001. TUDCA, tauroursodeoxycholic acid; ATF6, activating transcription factor 6; IRE1α, inositol-requiring enzyme 1 alpha; ATF4, activating transcription factor 4; CHOP, C/EBP homologous protein; GADD34, growth arrest and DNA damage-inducible protein 34; Bax, Bcl-2-associated X protein; Bcl2, B-cell lymphoma 2; Caspase 3, cysteine-aspartic acid protease 3; Caspase 9, cysteine-aspartic acid protease 9; PARP, poly(ADP-ribose) polymerase.

    Techniques Used:



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    Myrrh reduces the growth of human endometriotic cells by activating apoptotic signaling pathways. Endometriotic cells (12Z) and normal endometrial cells (T-HESC) were treated with the indicated concentrations of myrrh. (A) Cell viability was analyzed by measuring at 450 nm wavelength using MTT after 24 h. (B) To assess apoptotic or dead cell populations, 12Z cells were treated with increasing doses of myrrh for 24 h, and the percentages of Annexin V-positive and PI-positive cells were measured (Annexin V: Ex 494/Em 525 nm; PI: Ex 535/Em 617 nm). After 24 h of treatment with each concentration of myrrh, mitochondria-associated apoptotic proteins were analyzed by immunoblotting. (C) Representatives immunoblot images of Bax and Bcl-2 are shown. (D) A major monomeric Bax band at ~21 kDa (monomer Bax) and higher-molecular-weight bands corresponding to oligomeric forms (tetramer Bax, ~84 kDa) are indicated. (E) Representative immunoblot images of caspase-3, caspase-9 and PARP are shown. GAPDH was used as an internal control. (F) Densitometric analysis of protein levels. Data are expressed as relative intensity compared to control. Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. * P<0.05, ** P<0.01 and *** P<0.001. Ex, excitation; Em, emission; ; PARP, <t>poly(ADP-ribose)</t> <t>polymerase.</t>
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    Myrrh reduces the growth of human endometriotic cells by activating apoptotic signaling pathways. Endometriotic cells (12Z) and normal endometrial cells (T-HESC) were treated with the indicated concentrations of myrrh. (A) Cell viability was analyzed by measuring at 450 nm wavelength using MTT after 24 h. (B) To assess apoptotic or dead cell populations, 12Z cells were treated with increasing doses of myrrh for 24 h, and the percentages of Annexin V-positive and PI-positive cells were measured (Annexin V: Ex 494/Em 525 nm; PI: Ex 535/Em 617 nm). After 24 h of treatment with each concentration of myrrh, mitochondria-associated apoptotic proteins were analyzed by immunoblotting. (C) Representatives immunoblot images of Bax and Bcl-2 are shown. (D) A major monomeric Bax band at ~21 kDa (monomer Bax) and higher-molecular-weight bands corresponding to oligomeric forms (tetramer Bax, ~84 kDa) are indicated. (E) Representative immunoblot images of caspase-3, caspase-9 and PARP are shown. GAPDH was used as an internal control. (F) Densitometric analysis of protein levels. Data are expressed as relative intensity compared to control. Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. * P<0.05, ** P<0.01 and *** P<0.001. Ex, excitation; Em, emission; ; PARP, <t>poly(ADP-ribose)</t> <t>polymerase.</t>
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    Myrrh reduces the growth of human endometriotic cells by activating apoptotic signaling pathways. Endometriotic cells (12Z) and normal endometrial cells (T-HESC) were treated with the indicated concentrations of myrrh. (A) Cell viability was analyzed by measuring at 450 nm wavelength using MTT after 24 h. (B) To assess apoptotic or dead cell populations, 12Z cells were treated with increasing doses of myrrh for 24 h, and the percentages of Annexin V-positive and PI-positive cells were measured (Annexin V: Ex 494/Em 525 nm; PI: Ex 535/Em 617 nm). After 24 h of treatment with each concentration of myrrh, mitochondria-associated apoptotic proteins were analyzed by immunoblotting. (C) Representatives immunoblot images of Bax and Bcl-2 are shown. (D) A major monomeric Bax band at ~21 kDa (monomer Bax) and higher-molecular-weight bands corresponding to oligomeric forms (tetramer Bax, ~84 kDa) are indicated. (E) Representative immunoblot images of caspase-3, caspase-9 and PARP are shown. GAPDH was used as an internal control. (F) Densitometric analysis of protein levels. Data are expressed as relative intensity compared to control. Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. * P<0.05, ** P<0.01 and *** P<0.001. Ex, excitation; Em, emission; ; PARP, poly(ADP-ribose) polymerase.

    Journal: Experimental and Therapeutic Medicine

    Article Title: Myrrh ameliorates endometriosis by enhancing ER stress-related apoptotic cell death

    doi: 10.3892/etm.2026.13080

    Figure Lengend Snippet: Myrrh reduces the growth of human endometriotic cells by activating apoptotic signaling pathways. Endometriotic cells (12Z) and normal endometrial cells (T-HESC) were treated with the indicated concentrations of myrrh. (A) Cell viability was analyzed by measuring at 450 nm wavelength using MTT after 24 h. (B) To assess apoptotic or dead cell populations, 12Z cells were treated with increasing doses of myrrh for 24 h, and the percentages of Annexin V-positive and PI-positive cells were measured (Annexin V: Ex 494/Em 525 nm; PI: Ex 535/Em 617 nm). After 24 h of treatment with each concentration of myrrh, mitochondria-associated apoptotic proteins were analyzed by immunoblotting. (C) Representatives immunoblot images of Bax and Bcl-2 are shown. (D) A major monomeric Bax band at ~21 kDa (monomer Bax) and higher-molecular-weight bands corresponding to oligomeric forms (tetramer Bax, ~84 kDa) are indicated. (E) Representative immunoblot images of caspase-3, caspase-9 and PARP are shown. GAPDH was used as an internal control. (F) Densitometric analysis of protein levels. Data are expressed as relative intensity compared to control. Data are expressed as mean ± standard error of the mean. Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. * P<0.05, ** P<0.01 and *** P<0.001. Ex, excitation; Em, emission; ; PARP, poly(ADP-ribose) polymerase.

    Article Snippet: Subsequently. the membranes were subjected to overnight incubated at 4 ̊C with primary antibodies, including anti-human poly (ADP-ribose) polymerase (PARP, #9542s; Cell Signaling Technology, Inc.), caspases-3 (#9665s; Cell Signaling Technology, Inc.), caspase-9 (#9508s; Cell Signaling Technology, Inc.), Bax (NB100-56095; Novus Biologicals), Bcl-2 (NB100-56098; Novus Biologicals), p53 (sc-6243; Santa Cruz Biotechnology, Inc.) and glyceraldehyde 3-phosphate dehydrogenase (GAPDH, sc-32233; Santa Cruz Biotechnology, Inc.).

    Techniques: Protein-Protein interactions, Concentration Assay, Western Blot, Molecular Weight, Control

    Mechanism of action of myrrh in endometriosis. (A) 12Z were treated with the indicated concentrations of myrrh and TUDCA (200 µM). Cell viability was analyzed using MTT after 24 h, measured at a wavelength of 450 nm. (B) Schematic representation summarizing the experimental results and the potential mechanism by which myrrh exerts palliative effects on endometriosis. *** P<0.001. TUDCA, tauroursodeoxycholic acid; ATF6, activating transcription factor 6; IRE1α, inositol-requiring enzyme 1 alpha; ATF4, activating transcription factor 4; CHOP, C/EBP homologous protein; GADD34, growth arrest and DNA damage-inducible protein 34; Bax, Bcl-2-associated X protein; Bcl2, B-cell lymphoma 2; Caspase 3, cysteine-aspartic acid protease 3; Caspase 9, cysteine-aspartic acid protease 9; PARP, poly(ADP-ribose) polymerase.

    Journal: Experimental and Therapeutic Medicine

    Article Title: Myrrh ameliorates endometriosis by enhancing ER stress-related apoptotic cell death

    doi: 10.3892/etm.2026.13080

    Figure Lengend Snippet: Mechanism of action of myrrh in endometriosis. (A) 12Z were treated with the indicated concentrations of myrrh and TUDCA (200 µM). Cell viability was analyzed using MTT after 24 h, measured at a wavelength of 450 nm. (B) Schematic representation summarizing the experimental results and the potential mechanism by which myrrh exerts palliative effects on endometriosis. *** P<0.001. TUDCA, tauroursodeoxycholic acid; ATF6, activating transcription factor 6; IRE1α, inositol-requiring enzyme 1 alpha; ATF4, activating transcription factor 4; CHOP, C/EBP homologous protein; GADD34, growth arrest and DNA damage-inducible protein 34; Bax, Bcl-2-associated X protein; Bcl2, B-cell lymphoma 2; Caspase 3, cysteine-aspartic acid protease 3; Caspase 9, cysteine-aspartic acid protease 9; PARP, poly(ADP-ribose) polymerase.

    Article Snippet: Subsequently. the membranes were subjected to overnight incubated at 4 ̊C with primary antibodies, including anti-human poly (ADP-ribose) polymerase (PARP, #9542s; Cell Signaling Technology, Inc.), caspases-3 (#9665s; Cell Signaling Technology, Inc.), caspase-9 (#9508s; Cell Signaling Technology, Inc.), Bax (NB100-56095; Novus Biologicals), Bcl-2 (NB100-56098; Novus Biologicals), p53 (sc-6243; Santa Cruz Biotechnology, Inc.) and glyceraldehyde 3-phosphate dehydrogenase (GAPDH, sc-32233; Santa Cruz Biotechnology, Inc.).

    Techniques: