p16 cat Search Results


90
Spring Bioscience anti-human rabbit anti-p16 polyclonal antibody (spring™ bioscience; cat # e3284)
Anti Human Rabbit Anti P16 Polyclonal Antibody (Spring™ Bioscience; Cat # E3284), supplied by Spring Bioscience, 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/anti-human rabbit anti-p16 polyclonal antibody (spring™ bioscience; cat # e3284)/product/Spring Bioscience
Average 90 stars, based on 1 article reviews
anti-human rabbit anti-p16 polyclonal antibody (spring™ bioscience; cat # e3284) - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

90
Arigo Biolaboratories anti-p16 ink4a (cat. no. arg57377)
Honokiol (Hnk) protects H9c2 cardiomyocytes against Dox-induced senescence. (A) H9c2 cardiomyocytes were pretreated with different concentrations of Hnk (0.5-10 µ M) for 24 h prior to Dox (0.1 µ M) exposure for 48 h, which was followed by a CCK-8 assay to evaluate cell viability. (B) Cultured H9c2 cardiomyocytes were pretreated with Hnk (0, 2.5 or 5 µ M), followed by treatment with Dox (0.1 µ M) for 48 h. Representative images of the co-staining for SA-β-gal-positive cells (blue; arrows). Magnification ×200. Scale bar, 50 µ m. (C) Percentage of SA-β-gal-positive H9c2 cells. (D) Detection of <t>p16</t> <t>INK4A</t> and p21 protein levels. (E and F) Quantification of p16 INK4A and p21 protein levels. The results are representative of at least three independent experiments. &&& P<0.001 vs. vehicle group; * P<0.05, ** P<0.01, *** P<0.001 vs. Dox group. SA-β-gal, senescence-associated β-galactosidase; Dox, doxorubicin; Hnk2.5, honokiol 2.5 µ M; Hnk5.0, honokiol 5 µ M.
Anti P16 Ink4a (Cat. No. Arg57377), supplied by Arigo Biolaboratories, 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/anti-p16 ink4a (cat. no. arg57377)/product/Arigo Biolaboratories
Average 90 stars, based on 1 article reviews
anti-p16 ink4a (cat. no. arg57377) - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

90
Becton Dickinson monoclonal mouse anti-human p16 antibody cat. no. 550834
Honokiol (Hnk) protects H9c2 cardiomyocytes against Dox-induced senescence. (A) H9c2 cardiomyocytes were pretreated with different concentrations of Hnk (0.5-10 µ M) for 24 h prior to Dox (0.1 µ M) exposure for 48 h, which was followed by a CCK-8 assay to evaluate cell viability. (B) Cultured H9c2 cardiomyocytes were pretreated with Hnk (0, 2.5 or 5 µ M), followed by treatment with Dox (0.1 µ M) for 48 h. Representative images of the co-staining for SA-β-gal-positive cells (blue; arrows). Magnification ×200. Scale bar, 50 µ m. (C) Percentage of SA-β-gal-positive H9c2 cells. (D) Detection of <t>p16</t> <t>INK4A</t> and p21 protein levels. (E and F) Quantification of p16 INK4A and p21 protein levels. The results are representative of at least three independent experiments. &&& P<0.001 vs. vehicle group; * P<0.05, ** P<0.01, *** P<0.001 vs. Dox group. SA-β-gal, senescence-associated β-galactosidase; Dox, doxorubicin; Hnk2.5, honokiol 2.5 µ M; Hnk5.0, honokiol 5 µ M.
Monoclonal Mouse Anti Human P16 Antibody Cat. No. 550834, supplied by Becton Dickinson, 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/monoclonal mouse anti-human p16 antibody cat. no. 550834/product/Becton Dickinson
Average 90 stars, based on 1 article reviews
monoclonal mouse anti-human p16 antibody cat. no. 550834 - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

Image Search Results


Honokiol (Hnk) protects H9c2 cardiomyocytes against Dox-induced senescence. (A) H9c2 cardiomyocytes were pretreated with different concentrations of Hnk (0.5-10 µ M) for 24 h prior to Dox (0.1 µ M) exposure for 48 h, which was followed by a CCK-8 assay to evaluate cell viability. (B) Cultured H9c2 cardiomyocytes were pretreated with Hnk (0, 2.5 or 5 µ M), followed by treatment with Dox (0.1 µ M) for 48 h. Representative images of the co-staining for SA-β-gal-positive cells (blue; arrows). Magnification ×200. Scale bar, 50 µ m. (C) Percentage of SA-β-gal-positive H9c2 cells. (D) Detection of p16 INK4A and p21 protein levels. (E and F) Quantification of p16 INK4A and p21 protein levels. The results are representative of at least three independent experiments. &&& P<0.001 vs. vehicle group; * P<0.05, ** P<0.01, *** P<0.001 vs. Dox group. SA-β-gal, senescence-associated β-galactosidase; Dox, doxorubicin; Hnk2.5, honokiol 2.5 µ M; Hnk5.0, honokiol 5 µ M.

Journal: International Journal of Molecular Medicine

Article Title: Honokiol antagonizes doxorubicin-induced cardiomyocyte senescence by inhibiting TXNIP-mediated NLRP3 inflammasome activation

doi: 10.3892/ijmm.2019.4393

Figure Lengend Snippet: Honokiol (Hnk) protects H9c2 cardiomyocytes against Dox-induced senescence. (A) H9c2 cardiomyocytes were pretreated with different concentrations of Hnk (0.5-10 µ M) for 24 h prior to Dox (0.1 µ M) exposure for 48 h, which was followed by a CCK-8 assay to evaluate cell viability. (B) Cultured H9c2 cardiomyocytes were pretreated with Hnk (0, 2.5 or 5 µ M), followed by treatment with Dox (0.1 µ M) for 48 h. Representative images of the co-staining for SA-β-gal-positive cells (blue; arrows). Magnification ×200. Scale bar, 50 µ m. (C) Percentage of SA-β-gal-positive H9c2 cells. (D) Detection of p16 INK4A and p21 protein levels. (E and F) Quantification of p16 INK4A and p21 protein levels. The results are representative of at least three independent experiments. &&& P<0.001 vs. vehicle group; * P<0.05, ** P<0.01, *** P<0.001 vs. Dox group. SA-β-gal, senescence-associated β-galactosidase; Dox, doxorubicin; Hnk2.5, honokiol 2.5 µ M; Hnk5.0, honokiol 5 µ M.

Article Snippet: Anti-p16 INK4A (cat. no. ARG57377) was from Arigo Biolaboratories.

Techniques: CCK-8 Assay, Cell Culture, Staining

TXNIP gene silencing enhances the effect of honokiol (Hnk) treatment on Dox-induced senescence in H9c2 cardiomyocytes. Cultured H9c2 cardio-myocytes were infected with Ad-shNC or Ad-shTXNIP for 48 h, followed by treatment with Hnk (5 µ M) for 24 h, and then exposure to Dox (0.1 µ M) for 48 h. (A) mRNA levels of TXNIP in H9c2 cells infected with TXNIP knockdown adenovirus. (B and C) Detection of TXNIP protein levels and quantitative analysis. (D-G) Detection of relative TXNIP, NLRP3, caspase-1 and IL-1β mRNA levels. (H) Representative images of the co-staining for SA-β-gal-positive cells (blue; black arrows). Magnification ×200. Scale bar, 50 µ m. (I) Percentage of SA-β-gal-positive H9c2 cells. (J) Detection of p16 INK4A and p21 protein levels. (K and L) Quantification of p21 and p16 INK4A protein levels. The results are representative of at least three independent experiments. & P<0.05, &&& P<0.001 vs. vehicle group. *** P<0.001 vs. Dox group. $ P<0.05, $$ P<0.01, $$$ P<0.001 vs. Dox + Hnk group. Ad, adenovirus; SA-β-gal, senescence-associated β-galactosidase; Dox, doxorubicin; Hnk, honokiol 5 µ M; TXNIP, thioredoxin-interacting protein; NLRP3, NOD-like receptor family pyrin domain-containing 3; IL, interleukin.

Journal: International Journal of Molecular Medicine

Article Title: Honokiol antagonizes doxorubicin-induced cardiomyocyte senescence by inhibiting TXNIP-mediated NLRP3 inflammasome activation

doi: 10.3892/ijmm.2019.4393

Figure Lengend Snippet: TXNIP gene silencing enhances the effect of honokiol (Hnk) treatment on Dox-induced senescence in H9c2 cardiomyocytes. Cultured H9c2 cardio-myocytes were infected with Ad-shNC or Ad-shTXNIP for 48 h, followed by treatment with Hnk (5 µ M) for 24 h, and then exposure to Dox (0.1 µ M) for 48 h. (A) mRNA levels of TXNIP in H9c2 cells infected with TXNIP knockdown adenovirus. (B and C) Detection of TXNIP protein levels and quantitative analysis. (D-G) Detection of relative TXNIP, NLRP3, caspase-1 and IL-1β mRNA levels. (H) Representative images of the co-staining for SA-β-gal-positive cells (blue; black arrows). Magnification ×200. Scale bar, 50 µ m. (I) Percentage of SA-β-gal-positive H9c2 cells. (J) Detection of p16 INK4A and p21 protein levels. (K and L) Quantification of p21 and p16 INK4A protein levels. The results are representative of at least three independent experiments. & P<0.05, &&& P<0.001 vs. vehicle group. *** P<0.001 vs. Dox group. $ P<0.05, $$ P<0.01, $$$ P<0.001 vs. Dox + Hnk group. Ad, adenovirus; SA-β-gal, senescence-associated β-galactosidase; Dox, doxorubicin; Hnk, honokiol 5 µ M; TXNIP, thioredoxin-interacting protein; NLRP3, NOD-like receptor family pyrin domain-containing 3; IL, interleukin.

Article Snippet: Anti-p16 INK4A (cat. no. ARG57377) was from Arigo Biolaboratories.

Techniques: Cell Culture, Infection, Staining

TXNIP overexpression abrogates the effect of honokiol (Hnk) treatment on Dox-induced senescence in H9c2 cardiomyocytes. Cultured H9c2 cardiomyocytes were transfected with Ad-NC or Ad-TXNIP for 48 h, followed by treatment with Hnk (5 µ M) for 24 h and subsequent exposure to Dox (0.1 µ M) for 48 h. (A) mRNA levels of TXNIP in H9c2 cells infected with TXNIP overexpression adenovirus. (B and C) Detection of TXNIP protein levels and quantitative analysis. (D-G) Detection of relative TXNIP, NLRP3, caspase-1 and IL-1β mRNA levels. (H) Representative images of co-staining for SA-β-gal-positive cells (blue; arrows). Magnification ×200. Scale bars, 50 µ m. (I) Percentage of SA-β-gal-positive H9c2 cells. (J) Detection of p16 INK4A and p21 protein levels. (K and L) Quantification of p21 and p16 INK4A protein levels. The results are representative of at least three independent experiments. & P<0.05, && P<0.01, &&& P<0.001 vs. vehicle group; ** P<0.01, *** P<0.001 vs. Dox group; $$ P<0.01, $$$ P<0.001 vs. Dox + Hnk group. Ad, adenovirus; SA-β-gal, senescence-associated β-galactosidase; Dox, doxorubicin; Hnk, honokiol 5 µ M; TXNIP, thioredoxin-interacting protein; NLRP3, NOD-like receptor family pyrin domain-containing 3; IL, interleukin.

Journal: International Journal of Molecular Medicine

Article Title: Honokiol antagonizes doxorubicin-induced cardiomyocyte senescence by inhibiting TXNIP-mediated NLRP3 inflammasome activation

doi: 10.3892/ijmm.2019.4393

Figure Lengend Snippet: TXNIP overexpression abrogates the effect of honokiol (Hnk) treatment on Dox-induced senescence in H9c2 cardiomyocytes. Cultured H9c2 cardiomyocytes were transfected with Ad-NC or Ad-TXNIP for 48 h, followed by treatment with Hnk (5 µ M) for 24 h and subsequent exposure to Dox (0.1 µ M) for 48 h. (A) mRNA levels of TXNIP in H9c2 cells infected with TXNIP overexpression adenovirus. (B and C) Detection of TXNIP protein levels and quantitative analysis. (D-G) Detection of relative TXNIP, NLRP3, caspase-1 and IL-1β mRNA levels. (H) Representative images of co-staining for SA-β-gal-positive cells (blue; arrows). Magnification ×200. Scale bars, 50 µ m. (I) Percentage of SA-β-gal-positive H9c2 cells. (J) Detection of p16 INK4A and p21 protein levels. (K and L) Quantification of p21 and p16 INK4A protein levels. The results are representative of at least three independent experiments. & P<0.05, && P<0.01, &&& P<0.001 vs. vehicle group; ** P<0.01, *** P<0.001 vs. Dox group; $$ P<0.01, $$$ P<0.001 vs. Dox + Hnk group. Ad, adenovirus; SA-β-gal, senescence-associated β-galactosidase; Dox, doxorubicin; Hnk, honokiol 5 µ M; TXNIP, thioredoxin-interacting protein; NLRP3, NOD-like receptor family pyrin domain-containing 3; IL, interleukin.

Article Snippet: Anti-p16 INK4A (cat. no. ARG57377) was from Arigo Biolaboratories.

Techniques: Over Expression, Cell Culture, Transfection, Infection, Staining