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cyclin dependent kinase inhibitor 2a p16ink4a p16  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology cyclin dependent kinase inhibitor 2a p16ink4a p16
    LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers <t>(P16,</t> P53). (E–G) Assessment of stemness (SOX2) and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.
    Cyclin Dependent Kinase Inhibitor 2a P16ink4a P16, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 2157 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p16+antibody/pmc12813888-123-49-56?v=Santa+Cruz+Biotechnology
    Average 96 stars, based on 2157 article reviews
    cyclin dependent kinase inhibitor 2a p16ink4a p16 - by Bioz Stars, 2026-08
    96/100 stars

    Images

    1) Product Images from "On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation"

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2026.01.004

    LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers (P16, P53). (E–G) Assessment of stemness (SOX2) and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.
    Figure Legend Snippet: LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers (P16, P53). (E–G) Assessment of stemness (SOX2) and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.

    Techniques Used: Immunofluorescence, Staining, Quantitative RT-PCR, Inhibition

    LT-NPs-NIR modulate macrophage polarization and enhance TSPC-mediated tenogenic repair in a Transwell co-culture system. (A) Schematic of the Transwell co-culture setup. (B) SA-β-gal staining of macrophages. (C–F) Immunofluorescence of TSPCs for (C) P16, (D) SOX2, (E) SCX, and (F) Tenomodulin (TNMD) with F-actin. (G) Quantification of P16, SOX2, SCX, and TNMD levels. (H) Proposed mechanism: LT-NPs-NIR promote an M1-to-M2 macrophage shift and regulate TSPC senescence/stemness balance to favor tenogenic repair, potentially via STING/NF-κB signaling. Scale bars: 100 μm (B); 50 μm (C–E); 100 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
    Figure Legend Snippet: LT-NPs-NIR modulate macrophage polarization and enhance TSPC-mediated tenogenic repair in a Transwell co-culture system. (A) Schematic of the Transwell co-culture setup. (B) SA-β-gal staining of macrophages. (C–F) Immunofluorescence of TSPCs for (C) P16, (D) SOX2, (E) SCX, and (F) Tenomodulin (TNMD) with F-actin. (G) Quantification of P16, SOX2, SCX, and TNMD levels. (H) Proposed mechanism: LT-NPs-NIR promote an M1-to-M2 macrophage shift and regulate TSPC senescence/stemness balance to favor tenogenic repair, potentially via STING/NF-κB signaling. Scale bars: 100 μm (B); 50 μm (C–E); 100 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Techniques Used: Co-Culture Assay, Staining, Immunofluorescence

    Molecular assessment of tendon repair and systemic biosafety. (A) Representative immunofluorescence images of inflammatory, matrix-degrading, tenogenic, and senescence markers, alongside macrophage phenotypes in repaired tendons. (B) Correlation analysis integrating molecular and functional recovery. Bar charts (left Y-axis) display the relative fluorescence intensity of the indicated markers, overlaid with line graphs (right Y-axis) showing the fold change in biomechanical properties (Ultimate Load and Tensile Modulus). Note the inverse correlation between SASP factors (IL-6, MMP13, P16) and mechanical strength. (C) Western blot analysis of the STING pathway, senescence indicators, and heterotopic ossification markers (OCN, SOX9, BMP-2). (D, E) Systemic biosafety evaluation via H&E staining of major organs (D) and blood biochemistry analysis (E) showing no toxicity. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
    Figure Legend Snippet: Molecular assessment of tendon repair and systemic biosafety. (A) Representative immunofluorescence images of inflammatory, matrix-degrading, tenogenic, and senescence markers, alongside macrophage phenotypes in repaired tendons. (B) Correlation analysis integrating molecular and functional recovery. Bar charts (left Y-axis) display the relative fluorescence intensity of the indicated markers, overlaid with line graphs (right Y-axis) showing the fold change in biomechanical properties (Ultimate Load and Tensile Modulus). Note the inverse correlation between SASP factors (IL-6, MMP13, P16) and mechanical strength. (C) Western blot analysis of the STING pathway, senescence indicators, and heterotopic ossification markers (OCN, SOX9, BMP-2). (D, E) Systemic biosafety evaluation via H&E staining of major organs (D) and blood biochemistry analysis (E) showing no toxicity. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Techniques Used: Immunofluorescence, Functional Assay, Fluorescence, Western Blot, Staining



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    Image Search Results


    LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers (P16, P53). (E–G) Assessment of stemness (SOX2) and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.

    Journal: Bioactive Materials

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    doi: 10.1016/j.bioactmat.2026.01.004

    Figure Lengend Snippet: LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers (P16, P53). (E–G) Assessment of stemness (SOX2) and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.

    Article Snippet: After washing, cells were incubated with primary antibodies against Ki67 (ab15580, Abcam), Phosphorylated Histone H2AX (γ-H2AX) (ab81299, Abcam), SOX2 (sc-365964, Santa Cruz), Type I Collagen (COL1) (ab138492, Abcam), tenomodulin (TNMD) (ab203676, Abcam; sc-51813, Santa Cruz), Scleraxis (SCX) (sc-518082, Santa Cruz), IRF3 (ab68481, Abcam), Transcription Factor p65/RELA (P65) (A22331, Abclonal), Cyclin-Dependent Kinase Inhibitor 2A (p16INK4a) (P16) (sc-1661, Santa Cruz), P53 (10442-1-AP, Proteintech), Inducible Nitric Oxide Synthase (iNOS) (ab178945, Abcam), Arginase-1(Arg-1) (ab96183, Abcam), HSP70 (sc-32239, Santa Cruz), IL-6 (ab233706, Abcam), Matrix Metalloproteinase 13 (MMP13) (ab39012, Abcam), Double-stranded DNA (dsDNA) Marker (sc-58749, Santa Cruz), and Translocase of Outer Mitochondrial Membrane 20 (TOMM20) (11802-1-AP, Proteintech).

    Techniques: Immunofluorescence, Staining, Quantitative RT-PCR, Inhibition

    LT-NPs-NIR modulate macrophage polarization and enhance TSPC-mediated tenogenic repair in a Transwell co-culture system. (A) Schematic of the Transwell co-culture setup. (B) SA-β-gal staining of macrophages. (C–F) Immunofluorescence of TSPCs for (C) P16, (D) SOX2, (E) SCX, and (F) Tenomodulin (TNMD) with F-actin. (G) Quantification of P16, SOX2, SCX, and TNMD levels. (H) Proposed mechanism: LT-NPs-NIR promote an M1-to-M2 macrophage shift and regulate TSPC senescence/stemness balance to favor tenogenic repair, potentially via STING/NF-κB signaling. Scale bars: 100 μm (B); 50 μm (C–E); 100 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Journal: Bioactive Materials

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    doi: 10.1016/j.bioactmat.2026.01.004

    Figure Lengend Snippet: LT-NPs-NIR modulate macrophage polarization and enhance TSPC-mediated tenogenic repair in a Transwell co-culture system. (A) Schematic of the Transwell co-culture setup. (B) SA-β-gal staining of macrophages. (C–F) Immunofluorescence of TSPCs for (C) P16, (D) SOX2, (E) SCX, and (F) Tenomodulin (TNMD) with F-actin. (G) Quantification of P16, SOX2, SCX, and TNMD levels. (H) Proposed mechanism: LT-NPs-NIR promote an M1-to-M2 macrophage shift and regulate TSPC senescence/stemness balance to favor tenogenic repair, potentially via STING/NF-κB signaling. Scale bars: 100 μm (B); 50 μm (C–E); 100 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Article Snippet: After washing, cells were incubated with primary antibodies against Ki67 (ab15580, Abcam), Phosphorylated Histone H2AX (γ-H2AX) (ab81299, Abcam), SOX2 (sc-365964, Santa Cruz), Type I Collagen (COL1) (ab138492, Abcam), tenomodulin (TNMD) (ab203676, Abcam; sc-51813, Santa Cruz), Scleraxis (SCX) (sc-518082, Santa Cruz), IRF3 (ab68481, Abcam), Transcription Factor p65/RELA (P65) (A22331, Abclonal), Cyclin-Dependent Kinase Inhibitor 2A (p16INK4a) (P16) (sc-1661, Santa Cruz), P53 (10442-1-AP, Proteintech), Inducible Nitric Oxide Synthase (iNOS) (ab178945, Abcam), Arginase-1(Arg-1) (ab96183, Abcam), HSP70 (sc-32239, Santa Cruz), IL-6 (ab233706, Abcam), Matrix Metalloproteinase 13 (MMP13) (ab39012, Abcam), Double-stranded DNA (dsDNA) Marker (sc-58749, Santa Cruz), and Translocase of Outer Mitochondrial Membrane 20 (TOMM20) (11802-1-AP, Proteintech).

    Techniques: Co-Culture Assay, Staining, Immunofluorescence

    Molecular assessment of tendon repair and systemic biosafety. (A) Representative immunofluorescence images of inflammatory, matrix-degrading, tenogenic, and senescence markers, alongside macrophage phenotypes in repaired tendons. (B) Correlation analysis integrating molecular and functional recovery. Bar charts (left Y-axis) display the relative fluorescence intensity of the indicated markers, overlaid with line graphs (right Y-axis) showing the fold change in biomechanical properties (Ultimate Load and Tensile Modulus). Note the inverse correlation between SASP factors (IL-6, MMP13, P16) and mechanical strength. (C) Western blot analysis of the STING pathway, senescence indicators, and heterotopic ossification markers (OCN, SOX9, BMP-2). (D, E) Systemic biosafety evaluation via H&E staining of major organs (D) and blood biochemistry analysis (E) showing no toxicity. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Journal: Bioactive Materials

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    doi: 10.1016/j.bioactmat.2026.01.004

    Figure Lengend Snippet: Molecular assessment of tendon repair and systemic biosafety. (A) Representative immunofluorescence images of inflammatory, matrix-degrading, tenogenic, and senescence markers, alongside macrophage phenotypes in repaired tendons. (B) Correlation analysis integrating molecular and functional recovery. Bar charts (left Y-axis) display the relative fluorescence intensity of the indicated markers, overlaid with line graphs (right Y-axis) showing the fold change in biomechanical properties (Ultimate Load and Tensile Modulus). Note the inverse correlation between SASP factors (IL-6, MMP13, P16) and mechanical strength. (C) Western blot analysis of the STING pathway, senescence indicators, and heterotopic ossification markers (OCN, SOX9, BMP-2). (D, E) Systemic biosafety evaluation via H&E staining of major organs (D) and blood biochemistry analysis (E) showing no toxicity. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Article Snippet: After washing, cells were incubated with primary antibodies against Ki67 (ab15580, Abcam), Phosphorylated Histone H2AX (γ-H2AX) (ab81299, Abcam), SOX2 (sc-365964, Santa Cruz), Type I Collagen (COL1) (ab138492, Abcam), tenomodulin (TNMD) (ab203676, Abcam; sc-51813, Santa Cruz), Scleraxis (SCX) (sc-518082, Santa Cruz), IRF3 (ab68481, Abcam), Transcription Factor p65/RELA (P65) (A22331, Abclonal), Cyclin-Dependent Kinase Inhibitor 2A (p16INK4a) (P16) (sc-1661, Santa Cruz), P53 (10442-1-AP, Proteintech), Inducible Nitric Oxide Synthase (iNOS) (ab178945, Abcam), Arginase-1(Arg-1) (ab96183, Abcam), HSP70 (sc-32239, Santa Cruz), IL-6 (ab233706, Abcam), Matrix Metalloproteinase 13 (MMP13) (ab39012, Abcam), Double-stranded DNA (dsDNA) Marker (sc-58749, Santa Cruz), and Translocase of Outer Mitochondrial Membrane 20 (TOMM20) (11802-1-AP, Proteintech).

    Techniques: Immunofluorescence, Functional Assay, Fluorescence, Western Blot, Staining