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bh3 interacting domain death agonist 10988 1 ap  (Proteintech)


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    Proteintech bh3 interacting domain death agonist 10988 1 ap
    Bh3 Interacting Domain Death Agonist 10988 1 Ap, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 40 article reviews
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    Bh3 Interacting Domain Death Agonist 10988 1 Ap, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
    Bh3 Interacting Domain Death Agonist Cat, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
    Bh3 Interacting Domain Death Agonist, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
    Bh3 Interacting Domain Death Agonist (Bid) And Tbid Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, <t>BH3</t> interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.
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    Proteintech interacting domain death agonist bid
    Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining <t>for</t> <t>SLC1A5,</t> <t>BID,</t> and APOA5 proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5, apolipoprotein A-V; CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
    Interacting Domain Death Agonist Bid, supplied by Proteintech, 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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    Proteintech bh3 interacting domain death agonist (bid) antibody
    Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining <t>for</t> <t>SLC1A5,</t> <t>BID,</t> and APOA5 proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5, apolipoprotein A-V; CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)
    Bh3 Interacting Domain Death Agonist (Bid) Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bh3 interacting domain death agonist (bid) antibody/product/Proteintech
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    Image Search Results


    Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, BH3 interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.

    Journal: Translational Cancer Research

    Article Title: Neochlorogenic acid inhibits gastric cancer cell growth through apoptosis and cell cycle arrest

    doi: 10.21037/tcr-2025-696

    Figure Lengend Snippet: Western blot analysis reveals NCA-mediated modulation of apoptosis-associated proteins in HGC-27 and NUGC-3 cells. Following a 48-hour treatment with control or NCA, the expression of BAX, CASP3, BID, CYCS, and BCL2 was examined by Western blotting. β-actin was used as a loading control. Protein levels were normalized to β-actin and expressed as fold changes relative to the untreated control group. Bar graphs depict the quantification of relative protein levels. Data represent mean ± standard deviation from three independent experiments (n=3). Statistical significance was determined by Student’s t -test. *, P<0.05; **, P<0.01; ***, P<0.001. BAX, BCL2-associated X protein; BCL2, B-cell lymphoma 2; BID, BH3 interacting domain death agonist; CASP3, cysteinyl aspartate specific proteinase 3; CYCS, cytochrome c, somatic; NCA, neochlorogenic acid.

    Article Snippet: The membranes were then incubated overnight at 4 °C with primary antibodies for BCL2 (B-cell lymphoma 2) (Cat. No. bs-0032R; Bioss, Beijing, China), BID (BH3 interacting domain death agonist) (Cat. No. 10988-1-AP), CYCS (cytochrome c, somatic) (Cat. No. 10993-1-AP) from Proteintech (Wuhan, China), as well as β-actin (Cat. No. 81115-1-RR, Proteintech, Wuhan, China) and BAX (BCL2-associated X protein) (Cat. No. 50599-2-Ig, Proteintech, Wuhan, China).

    Techniques: Western Blot, Control, Expressing, Standard Deviation

    Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and APOA5 proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5, apolipoprotein A-V; CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)

    Journal: Journal of Translational Medicine

    Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry

    doi: 10.1186/s12967-023-04723-1

    Figure Lengend Snippet: Validation of ferroptosis- and lipid metabolism-associated DEPs using IHC in a validation cohort. A Representative images (see Additional file : Figure S4a,b for 500 µm images) of immunohistochemical staining of TFR1, TF, AIFM2, DPP4, and GCLC proteins in stable and unstable plaques in the plaque fibrous cap region (black arrows) and immunohistochemical staining for SLC1A5, BID, and APOA5 proteins in the plaque lipid core region (black arrows). B In unstable plaques, the levels of TFR1, TF, AIFM2, DPP4, GCLC, SLC1A5, BID, and APOA5 were significantly increased, while other differences were not statistically significant. IHC immunohistochemistry. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic. SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5, apolipoprotein A-V; CETP cholesteryl ester transfer protein. *P < 0.05; **P < 0.01 Student’s t test (two-tailed distribution)

    Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and apolipoprotein A-V (APOA5) (rabbit polyclonal, 18019-1-AP) were purchased from Proteintech (China).

    Techniques: Biomarker Discovery, Immunohistochemical staining, Staining, Immunohistochemistry, Two Tailed Test

    The differently expressed proteins (DEPs) that were validated using immunohistochemistry (all up regulated) (unstable/stable)

    Journal: Journal of Translational Medicine

    Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry

    doi: 10.1186/s12967-023-04723-1

    Figure Lengend Snippet: The differently expressed proteins (DEPs) that were validated using immunohistochemistry (all up regulated) (unstable/stable)

    Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and apolipoprotein A-V (APOA5) (rabbit polyclonal, 18019-1-AP) were purchased from Proteintech (China).

    Techniques: Immunohistochemistry, Biomarker Discovery, Significance Assay

    Hypothetical characterization of altered molecular mechanisms in cells in the fibrous cap and lipid core regions of unstable carotid plaques. The expression of key proteins of ferroptosis and lipid metabolism is significantly increased in patients with unstable plaques, and there are mechanisms associated with both the promotion and inhibition of iron death. This possibly indicates that cells in different regions of the plaque are regulated by key proteins of ferroptosis that subsequently lead to increased plaque instability and expansion of the necrotic core. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic; SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5 apolipoprotein A-V; CETP cholesteryl ester transfer protein; GPX4 glutathione peroxidase 4; GSH glutathione; CoQ10 coenzyme Q10; ROS reactive oxygen species; HDL high-density lipoprotein; ox-LDL oxidized low-density lipoprotein

    Journal: Journal of Translational Medicine

    Article Title: Characterization of the proteome of stable and unstable carotid atherosclerotic plaques using data-independent acquisition mass spectrometry

    doi: 10.1186/s12967-023-04723-1

    Figure Lengend Snippet: Hypothetical characterization of altered molecular mechanisms in cells in the fibrous cap and lipid core regions of unstable carotid plaques. The expression of key proteins of ferroptosis and lipid metabolism is significantly increased in patients with unstable plaques, and there are mechanisms associated with both the promotion and inhibition of iron death. This possibly indicates that cells in different regions of the plaque are regulated by key proteins of ferroptosis that subsequently lead to increased plaque instability and expansion of the necrotic core. TFR1 transferrin receptor protein 1; TF transferrin; AIFM2 apoptosis-inducing factor 2; DPP4 dipeptidyl peptidase 4; GCLC glutamate-cysteine ligase catalytic; SLC1A5 solute carrier family 1, member 5; BID BH3 interacting-domain death agonist; APOA5 apolipoprotein A-V; CETP cholesteryl ester transfer protein; GPX4 glutathione peroxidase 4; GSH glutathione; CoQ10 coenzyme Q10; ROS reactive oxygen species; HDL high-density lipoprotein; ox-LDL oxidized low-density lipoprotein

    Article Snippet: Primary antibodies for IHC against solute carrier family 1, member 5 (SLC1A5) (rabbit polyclonal, 20350-1-AP), apoptosis-inducing factor 2 (AIFM2) (rabbit polyclonal, 20886–1-AP), BH3 interacting-domain death agonist (BID) (rabbit polyclonal, 10988-1-AP), dipeptidyl peptidase 4 (DPP4) (rabbit polyclonal, 29403-1-AP), transferrin receptor protein 1 (TFR1) (mouse monoclonal, 66180–1-Ig), transferrin (TF) (rabbit polyclonal, 17435-1-AP), glutamate–cysteine ligase catalytic (GCLC) (rabbit polyclonal, 12601–1-AP), cholesteryl ester transfer protein (CETP) (rabbit polyclonal, 13459-1-AP), and apolipoprotein A-V (APOA5) (rabbit polyclonal, 18019-1-AP) were purchased from Proteintech (China).

    Techniques: Expressing, Inhibition