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p16 ink4a  (Bioss)


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    Structured Review

    Bioss p16 ink4a
    CI in older and D‐gal‐induced mice is accompanied by microglial senescence and elevated ghrelin levels. (A) Experimental design of the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Young, Old, Control, and D‐gal groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Young and Old groups and from the Control and D‐gal groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers <t>p16</t> <t>Ink4a</t> , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Young, Old, Control, and D‐gal groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 and CA3 regions of the mice from Young, Old, Control, and D‐gal groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, CXCL10, LIF, MCP1, and M‐CSF) in the Young, Old, Control, and D‐gal groups. (I) ELISA measurement of plasma total ghrelin and acylated ghrelin in the Young, Old, Control, and D‐gal groups. ** p < 0.01, *** p < 0.001.
    P16 Ink4a, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+p16+antibodies/CDKN2A+p16-INK4a+Polyclonal+Antibody/pmc13621234-152-34-38
    Average 94 stars, based on 10 article reviews
    p16 ink4a - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "Ghrelin Alleviates Aging‐Related Cognitive Impairment by Regulating Autophagy‐Related Signaling via the SHBG / JNK1 /Beclin1 Axis in Microglia"

    Article Title: Ghrelin Alleviates Aging‐Related Cognitive Impairment by Regulating Autophagy‐Related Signaling via the SHBG / JNK1 /Beclin1 Axis in Microglia

    Journal: Aging Cell

    doi: 10.1111/acel.70732

    CI in older and D‐gal‐induced mice is accompanied by microglial senescence and elevated ghrelin levels. (A) Experimental design of the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Young, Old, Control, and D‐gal groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Young and Old groups and from the Control and D‐gal groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers p16 Ink4a , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Young, Old, Control, and D‐gal groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 and CA3 regions of the mice from Young, Old, Control, and D‐gal groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, CXCL10, LIF, MCP1, and M‐CSF) in the Young, Old, Control, and D‐gal groups. (I) ELISA measurement of plasma total ghrelin and acylated ghrelin in the Young, Old, Control, and D‐gal groups. ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: CI in older and D‐gal‐induced mice is accompanied by microglial senescence and elevated ghrelin levels. (A) Experimental design of the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Young, Old, Control, and D‐gal groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Young and Old groups and from the Control and D‐gal groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers p16 Ink4a , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Young, Old, Control, and D‐gal groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 and CA3 regions of the mice from Young, Old, Control, and D‐gal groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, CXCL10, LIF, MCP1, and M‐CSF) in the Young, Old, Control, and D‐gal groups. (I) ELISA measurement of plasma total ghrelin and acylated ghrelin in the Young, Old, Control, and D‐gal groups. ** p < 0.01, *** p < 0.001.

    Techniques Used: Control, Western Blot, Analysis, Tissue, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Clinical Proteomics

    Ghrelin administration alleviates D‐gal‐induced microglial senescence and CI. (A) Experimental design of ghrelin treatment in the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal+Ghrelin groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers p16 Ink4a , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Control, Control+Ghrelin, D‐gal, and D‐gal+Ghrelin groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 region of the mice from Control, Control+Ghrelin, D‐gal, and D‐gal + Ghrelin groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, IP10/CXCL10, LIF, MCP1, and M‐CSF) in the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups. *** p < 0.001.
    Figure Legend Snippet: Ghrelin administration alleviates D‐gal‐induced microglial senescence and CI. (A) Experimental design of ghrelin treatment in the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal+Ghrelin groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers p16 Ink4a , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Control, Control+Ghrelin, D‐gal, and D‐gal+Ghrelin groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 region of the mice from Control, Control+Ghrelin, D‐gal, and D‐gal + Ghrelin groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, IP10/CXCL10, LIF, MCP1, and M‐CSF) in the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups. *** p < 0.001.

    Techniques Used: Control, Western Blot, Analysis, Tissue, Immunofluorescence, Enzyme-linked Immunosorbent Assay

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    Incubation:

    Article Title: PDK1 inhibition reduces autophagy and cell senescence through the PI3K/AKT signalling pathway in a cigarette smoke mouse emphysema model
    Article Snippet: Slices was blocked with normal 5% goat serum (cat. no. AR1009; Wuhan Boster Biological Technology, Ltd.) for 30 min at room temperature. .. Slices were incubated with anti-LC3B (1:100; cat. no. APG8B; Abcepta) and anti-p16 antibodies (1:100; cat. no. Bs-11652R; BIOSS) overnight at 4 ̊C. .. The samples were then washed (PBST; Tween-20 0.05%; cat. no. P1031; Beijing Solarbio Science & Technology Co., Ltd.) extensively and incubated with the appropriate CY3-labeled goat anti-mouse IgG (1:100; cat. no. BA1031; Wuhan Boster Biological Technology) and goat anti-rabbit IgG (1:100; cat. no. BA1032; Wuhan Boster Biological Technology) HRP-conjugated secondary antibodies for 1 h at room temperature in the dark.



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    CI in older and D‐gal‐induced mice is accompanied by microglial senescence and elevated ghrelin levels. (A) Experimental design of the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Young, Old, Control, and D‐gal groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Young and Old groups and from the Control and D‐gal groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers <t>p16</t> <t>Ink4a</t> , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Young, Old, Control, and D‐gal groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 and CA3 regions of the mice from Young, Old, Control, and D‐gal groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, CXCL10, LIF, MCP1, and M‐CSF) in the Young, Old, Control, and D‐gal groups. (I) ELISA measurement of plasma total ghrelin and acylated ghrelin in the Young, Old, Control, and D‐gal groups. ** p < 0.01, *** p < 0.001.
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    CI in older and D‐gal‐induced mice is accompanied by microglial senescence and elevated ghrelin levels. (A) Experimental design of the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Young, Old, Control, and D‐gal groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Young and Old groups and from the Control and D‐gal groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers p16 Ink4a , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Young, Old, Control, and D‐gal groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 and CA3 regions of the mice from Young, Old, Control, and D‐gal groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, CXCL10, LIF, MCP1, and M‐CSF) in the Young, Old, Control, and D‐gal groups. (I) ELISA measurement of plasma total ghrelin and acylated ghrelin in the Young, Old, Control, and D‐gal groups. ** p < 0.01, *** p < 0.001.

    Journal: Aging Cell

    Article Title: Ghrelin Alleviates Aging‐Related Cognitive Impairment by Regulating Autophagy‐Related Signaling via the SHBG / JNK1 /Beclin1 Axis in Microglia

    doi: 10.1111/acel.70732

    Figure Lengend Snippet: CI in older and D‐gal‐induced mice is accompanied by microglial senescence and elevated ghrelin levels. (A) Experimental design of the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Young, Old, Control, and D‐gal groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Young and Old groups and from the Control and D‐gal groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Young and Old groups and from the Control and D‐gal groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers p16 Ink4a , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Young, Old, Control, and D‐gal groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 and CA3 regions of the mice from Young, Old, Control, and D‐gal groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, CXCL10, LIF, MCP1, and M‐CSF) in the Young, Old, Control, and D‐gal groups. (I) ELISA measurement of plasma total ghrelin and acylated ghrelin in the Young, Old, Control, and D‐gal groups. ** p < 0.01, *** p < 0.001.

    Article Snippet: Following antibody stripping and re‐blocking, sections were incubated overnight at 4°C with a second primary antibody: γH2AX (1:400; ab81299, Abcam), high‐mobility group box 1 (HMGB1) (1:400; AWA10032 , Abiowell), p21 Cip1 (1:200; ab188224, Abcam), p16 Ink4a (1:200; bs‐23797R, Bioss, China), or Lamin B1 (1:400; ab8982, Abcam).

    Techniques: Control, Western Blot, Analysis, Tissue, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Clinical Proteomics

    Ghrelin administration alleviates D‐gal‐induced microglial senescence and CI. (A) Experimental design of ghrelin treatment in the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal+Ghrelin groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers p16 Ink4a , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Control, Control+Ghrelin, D‐gal, and D‐gal+Ghrelin groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 region of the mice from Control, Control+Ghrelin, D‐gal, and D‐gal + Ghrelin groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, IP10/CXCL10, LIF, MCP1, and M‐CSF) in the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups. *** p < 0.001.

    Journal: Aging Cell

    Article Title: Ghrelin Alleviates Aging‐Related Cognitive Impairment by Regulating Autophagy‐Related Signaling via the SHBG / JNK1 /Beclin1 Axis in Microglia

    doi: 10.1111/acel.70732

    Figure Lengend Snippet: Ghrelin administration alleviates D‐gal‐induced microglial senescence and CI. (A) Experimental design of ghrelin treatment in the D‐gal‐induced aging mouse model. (B) Percentage change in body weight of mice in the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups, normalized to baseline body weight at the start of the experiment. (C) The NOL test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups. The recognition index was calculated as the ratio of time spent exploring in the novel location to the total time spent exploring both locations. (D) NOR test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal+Ghrelin groups. The recognition index was calculated as the ratio of time spent exploring the novel object relative to the total exploration time for both objects. (E) MWM test comparing the mice from the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups, including swimming trajectories and escape latency. (F) Western blot analysis of senescence markers p16 Ink4a , p21 Cip1 , LaminB1, γH2AX, and HMGB1 in the mice brain tissue from the Control, Control+Ghrelin, D‐gal, and D‐gal+Ghrelin groups. (G) Immunofluorescence co‐localization of Iba‐1 + microglia with LaminB1, γH2AX, and HMGB1 in the hippocampal CA1 region of the mice from Control, Control+Ghrelin, D‐gal, and D‐gal + Ghrelin groups (magnification: ×400, scale bar = 25 μm). (H) ELISA‐based quantification of hippocampal cytokines (IL‐1α, IL‐1β, G‐CSF, IL‐4, IL‐6, IL‐8, IP10/CXCL10, LIF, MCP1, and M‐CSF) in the Control, Control + Ghrelin, D‐gal, and D‐gal + Ghrelin groups. *** p < 0.001.

    Article Snippet: Following antibody stripping and re‐blocking, sections were incubated overnight at 4°C with a second primary antibody: γH2AX (1:400; ab81299, Abcam), high‐mobility group box 1 (HMGB1) (1:400; AWA10032 , Abiowell), p21 Cip1 (1:200; ab188224, Abcam), p16 Ink4a (1:200; bs‐23797R, Bioss, China), or Lamin B1 (1:400; ab8982, Abcam).

    Techniques: Control, Western Blot, Analysis, Tissue, Immunofluorescence, Enzyme-linked Immunosorbent Assay

    Journal: Cell Reports Medicine

    Article Title: A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration

    doi: 10.1016/j.xcrm.2026.102937

    Figure Lengend Snippet:

    Article Snippet: Rabbit Polyclonal anti-p16 , ABclonal , Cat# A11651; RRID: AB_2861619.

    Techniques: Recombinant, Lysis, Hydroxyproline Assay, Enzyme-linked Immunosorbent Assay, Isolation, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Staining, Software

    The antibodies used in this study

    Journal: Cellular & Molecular Biology Letters

    Article Title: Grx2 deficiency accelerates BMSC senescence and senile osteoporosis via CD36 S-glutathionylation

    doi: 10.1186/s11658-026-00999-5

    Figure Lengend Snippet: The antibodies used in this study

    Article Snippet: Anti-p16 , SANTA CRUZ, Sc1661 , Goat anti-rabbit IgG (488,594) , Protintech, SA00013-2 Protintech, SA00013-4.

    Techniques: