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Proteintech p53
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, <t>P53).</t> (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.
P53, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 2196 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 2196 article reviews
p53 - by Bioz Stars, 2026-10
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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

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Article Snippet: PFA-fixed samples were permeabilized (0.5% Triton X-100), blocked (5% BSA), and incubated with primary antibodies (SENP3, #5591, CST; ASS1, 16210-1-AP, Proteintech; LTL, L32480 , Invitrogen; P53, 60283-2-Ig, Proteintech) followed by DAPI.



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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, <t>P53).</t> (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.
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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, <t>P53).</t> (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.
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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, <t>P53).</t> (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.
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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, <t>P53).</t> (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.
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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, <t>P53).</t> (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.
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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, <t>P53).</t> (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.
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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, <t>P53).</t> (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.
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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