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 2195 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p16ink4a/p16+Antibody/pmc12813888-123-49-56
Average 96 stars, based on 2195 article reviews

cyclin dependent kinase inhibitor 2a p16ink4a p16 - by Bioz Stars, 2026-09

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

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

Incubation:

Article Title: Reevaluating the senolytic activity of a GLS1 inhibitor and an anti-PD-1 antibody: toward greater reproducibility and methodological rigor.
Article Snippet: Samples were denatured in Laemmli sample buffer by heating at 95 °C for 5 min. Proteins were separated by SDS–polyacrylamide gel electrophoresis and transferred onto PVDF membranes (IPVH00010, EMD Millipore). .. Membranes were blocked with 5% non-fat milk and incubated with the following primary antibodies: β-actin (1:2000; A5316, Sigma-Aldrich, 1:1000; A4700, Sigma-Aldrich), Lamin B1 (1:1000; ab16048, Abcam), p16INK4a (1:1000; sc-56330, Santa Cruz, 1:1000; 11104, IBL), and p21Waf1/Cip1 (1:1000; 2947, Cell Signaling Technology). .. After washing, membranes were incubated with HRP-conjugated secondary antibodies (1:2000; 7074 and 7076, Cell Signaling Technology) and developed using Amersham ECL Prime or Select reagents (RPN2236 or RPN2235, GE Healthcare).

Immunohistochemistry:

Article Title: Low-intensity pulsed ultrasound inhibits chondrocyte senescence by inhibiting PI3K/AKT/mTOR signaling
Article Snippet: .. The antibodies used included [p21, Abcam, ab188224, 1:1000; p16ink4a, Santa Cruz, SC-1661, 1:100; p53, Abcam, ab32049, 1:50; Lamin B1, Affinity, AF5161, 1:100; Collagen II, Affinity, AF0135,1:100; MMP-13, Affinity, AF5355, 1:100], which have been validated for use in IHC. .. Afterward, biotinylated secondary antibody [Goat Anti-Rabbit/Mouse IgG HRP, Abcam, ab6721/ab205719, 1:1000], and horseradish peroxidase-conjugated streptavidin were applied for 1 h at room temperature.

Staining:

Article Title: In Vitro Model Characterizing Carcinogenic Progression of HPV-Positive Oropharyngeal Cancer.
Article Snippet: .. Each sample was stained with antibodies against Keratin 5 (1:1000 dilution; catalog number MA5-12596; Invitrogen, Rockford, IL, USA), Keratin 10 (1:1000 dilution; catalog number MA1-06319; Invitrogen), Keratin 6 (1:1000 dilution; catalog number MS-766-P; NeoMarkers, Fremont, CA, USA), p53 (DO-1) (1:1000 dilution; catalog number sc-126; Santa Cruz Biotechnology, Paso Robles, CA, USA), Rb (Rb1) (1:1000 dilution; catalog number sc-73598; Santa Cruz Biotechnology), Keratin 8 (1:1000 dilution; catalog number MA5-14428; Invitrogen), p16INK4A (1:1000 dilution; catalog number sc-56330; Santa Cruz Biotechnology), COX5b (C-5) (1:1000 dilution; catalog number sc-374416; Santa Cruz Biotechnology), and p120 (6H11) (1:1000 dilution; catalog number sc-23873; Santa Cruz Biotechnology). .. The slides were then rinsed with TBS-Tween 3 times and stained with secondary antibody (Alexa Fluor 488; Life Technologies, Eugene, OR, USA) diluted 1:200 for 1 h at room temperature.

Article Title: Multiple synergistic anti-aging effects of vascular cell adhesion molecule 1 functionalized nanoplatform to improve age-related neurodegenerative diseases.
Article Snippet: Aging is a critical factor in the onset and progression of neurodegenerative diseases and cognitive decline, with aging-related neuroinflammation and cellular senescence being major contributors.. In the aging brain, the cerebral vascular endothelium overexpresses vascular cell adhesion molecule 1 (VCAM1), activating microglia and leading to neuroinflammation and cognitive impairment.. Quercetin, a natural neuroprotective agent widely used for treating neurodegenerative diseases, their therapeutic efficacy, however, is limited by its poor water solubility and inability to penetrate the blood-brain barrier (BBB).

Article Title: Senolytic-sensitive p16 Ink4a + fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity.
Article Snippet: Article Senolytic-sensitive p16 Ink4a + fibroblasts in the tumor stroma rewire lung cancer metabolism and plasticity

CCK-8 Assay:

ROS Assay:

Enzyme-linked Immunosorbent Assay:

other:

Article Title: Increased hydrogen sulfide turnover serves a cytoprotective role during the development of replicative senescence.
Article Snippet: The mammalian gasotransmitter hydrogen sulfide (H2S) is produced by enzymes such as cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), 3-mercaptopyruvate sulfurtransferase (3-MST).. Prior studies suggest that H2S may have cytoprotective and anti-aging effects.. This project explores the regulation and role of endogenous H2S in a murine model of replicative senescence.

Review