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anti poly  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti poly
    Anti Poly, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 15315 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+poly/PARP+Antibody/pmc12981022-105-23-30
    Average 98 stars, based on 15315 article reviews
    anti poly - by Bioz Stars, 2026-09
    98/100 stars

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    Related Articles

    other:

    Article Title: miR-145-5p/CAMSAP2 axis modulates cisplatin sensitivity in non-small cell lung cancer
    Article Snippet: Primary antibodies used were anti-CAMSAP2 (Proteintech #17880-1-AP, 1:1000), anti-Poly(ADP-ribose) Polymerase (PARP) (Cell Signaling Technology #9542, 1:1000), anti-actin (Cell Signaling Technology), anti-phosphorylate AKT (Cell Signaling Technology #9271, 1:1000), anti-AKT (Cell Signaling Technology #9272, 1:1000), anti-phosphorylate PI3K (Cell Signaling Technology #4228, 1:1000), anti-PI3K (Cell Signaling Technology #4257, 1:1000), anti-β-catenin (Cell Signaling Technology #8480, 1:1000), anti-phosphorylate GSK3β (Cell Signaling Technology #9336, 1:1000), anti-GSK3β (Cell Signaling Technology #9315, 1:1000), anti-Bcl-2 (Cell Signaling Technology #4223, 1:1000), anti-Bax (Cell Signaling Technology #2772, 1:1000), anti-GAPDH (Santacruz #sc-32233, 1:2000), HRP-conjugated anti-rabbit (Cell Signaling Technology #7074, 1:1000), and HRP-conjugated anti-mouse (Cell Signaling Technology #7076, 1:1000).

    Article Title: miR-145-5p/CAMSAP2 axis modulates cisplatin sensitivity in non-small cell lung cancer.
    Article Snippet: Primary antibodies used were anti-CAMSAP2 (Proteintech #17880-1-AP, 1:1000), anti-Poly(ADP-ribose) Polymerase (PARP) (Cell Signaling Technology #9542, 1:1000), anti-actin (Cell Signaling Technology), anti-phosphorylate AKT (Cell Signaling Technology #9271, 1:1000), anti-AKT (Cell Signaling Technology #9272, 1:1000), anti-phosphorylate PI3K (Cell Signaling Technology #4228, 1:1000), anti-PI3K (Cell Signaling Technology

    Article Title: Platycodin D sensitizes head and neck squamous cell carcinoma to cisplatin by inducing autophagy arrest.
    Article Snippet: The following antibodies were used: Anti‐LC3A/B (1:1,000; cat. no. 12741S; Cell Signaling Technology, Inc.), anti‐SQSTM1/p62 (1:1,000; cat. no. 5114S; Cell Signaling Technology, Inc.), anti‐poly(ADP‐ribose) polymerase (PARP; 1:1,000; cat. no. 9542S; Cell Signaling Technology, Inc.), anti‐caspase 3 (1:1,000; cat. no. 9662S; Cell Signaling Technology, Inc.) and anti‐β‐actin (1:5,000; cat. no. 47778; Santa Cruz Biotechnology, Inc.).

    Article Title: NSC777201 exhibits anticancer activity against colorectal cancer cells by inducing multiple types of cell death
    Article Snippet: Anti-GAPDH (A19056, 1:20000), anti-vinculin (A2752, 1:2000), anti-ferritin light chain (FTL; A11241, 1:5000), anti-EGFR (4267, 1:1000), anti-phospho-EGFR (2243, 1:1000), and anti-poly(ADP ribose) polymerase (PARP; 9542, 1:1000) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Article Title: Platycodin D sensitizes head and neck squamous cell carcinoma to cisplatin by inducing autophagy arrest
    Article Snippet: The following antibodies were used: Anti-LC3A/B (1:1,000; cat. no. 12741S; Cell Signaling Technology, Inc.), anti-SQSTM1/p62 (1:1,000; cat. no. 5114S; Cell Signaling Technology, Inc.), anti-poly(ADP-ribose) polymerase (PARP; 1:1,000; cat. no. 9542S; Cell Signaling Technology, Inc.), anti-caspase 3 (1:1,000; cat. no. 9662S; Cell Signaling Technology, Inc.) and anti-β-actin (1:5,000; cat. no. 47778; Santa Cruz Biotechnology, Inc.).

    Article Title: VPS35 Deficiency Markedly Reduces the Proliferation of HEK293 Cells
    Article Snippet: The following primary antibodies were used: anticaspase-3 (9662S; 1:3000), anti-poly(ADP-ribose) polymerase (PARP; 9542S; 1:3000), anticytochrome C (11940S; 1:1000), anti-CDK4 (12790S; 1:2000), anti-cyclinD1 (2978S; 1:3000), anti-Drp1 (8570S; 1:3000), and anti-pDrp1 (S616) (3455S; 1:1000) (all from Cell Signaling Technology, Danvers, MA, USA); anti-Ki-67 (ab15580; 1:1000; Abcam, Boston, MA, USA); anti-Mfn2 (sc-515647; 1:1000; Santa Cruz Biotechnology, Dallas, TX, USA); and anti-GAPDH (LF-PA0018; 1:3000; AbFrontier, Seoul, Republic of Korea).

    Article Title: VPS35 Deficiency Markedly Reduces the Proliferation of HEK293 Cells
    Article Snippet: The following primary antibodies were used: anti-caspase-3 (9662S; 1:3000), anti-poly(ADP-ribose) polymerase (PARP; 9542S; 1:3000), anticytochrome C (11940S; 1:1000), anti-CDK4 (12790S; 1:2000), anti-cyclinD1 (2978S; 1:3000), anti-Drp1 (8570S; 1:3000), and anti-pDrp1 (S616) (3455S; 1:1000) (all from Cell Signaling Technology, Danvers, MA, USA); anti-Ki-67 (ab15580; 1:1000; Abcam, Boston, MA, USA); anti-Mfn2 (sc-515647; 1:1000; Santa Cruz Biotechnology, Dallas, TX, USA); and anti-GAPDH (LF-PA0018; 1:3000; AbFrontier, Seoul, Republic of Korea).



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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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    Cell Signaling Technology Inc poly mono adp ribose antibody d9p7z
    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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    Image Search Results


    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: