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p16 ink4a  (Bioss)
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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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti p16ink4a  (Santa Cruz Biotechnology)
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Santa Cruz Biotechnology anti p16ink4a
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.
Anti P16ink4a, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p16 10883 1 ap rabbit  (Proteintech)
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Proteintech p16 10883 1 ap rabbit
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 10883 1 Ap Rabbit, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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antibodies against p16  (ABclonal Biotechnology)
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ABclonal Biotechnology antibodies against p16
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.
Antibodies Against P16, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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antibodies against p16 - by Bioz Stars, 2026-10
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p16  (Proteintech)
96
Proteintech p16
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, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p16/P16-INK4A+Antibody/pm42789189-98-75-78
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p21  (Proteintech)
96
Proteintech p21
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.
P21, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p16  (ABclonal Biotechnology)
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ABclonal Biotechnology p16
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, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti p16  (ABclonal Biotechnology)
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ABclonal Biotechnology anti p16
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.
Anti P16, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


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