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antibodies against lepr biotin  (R&D Systems)


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    R&D Systems antibodies against lepr biotin
    Antibodies Against Lepr Biotin, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 80 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/antibody+against+mouse+leptin/Mouse+Leptin+R+Biotinylated+Antibody/10__1016_slash_j__eng__2025__08__019-72-10-17
    Average 95 stars, based on 80 article reviews
    antibodies against lepr biotin - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Injection:

    Article Title: Leptin derived from adipocytes in injured peripheral nerves facilitates development of neuropathic pain via macrophage stimulation
    Article Snippet: .. A single injection of 10 μL of recombinant mouse leptin (1 μg) or a neutralizing antibody against mouse leptin (1 ng; R & D Systems) was given to mouse SCN immediately after PSL and 3 h before behavioral testing, once daily. .. Vehicle (PBS) or normal goat IgG (10 ng; R & D Systems) was given to the control groups for leptin treatment or the neutralizing antibody, respectively.

    Recombinant:

    Article Title: Leptin derived from adipocytes in injured peripheral nerves facilitates development of neuropathic pain via macrophage stimulation
    Article Snippet: .. A single injection of 10 μL of recombinant mouse leptin (1 μg) or a neutralizing antibody against mouse leptin (1 ng; R & D Systems) was given to mouse SCN immediately after PSL and 3 h before behavioral testing, once daily. .. Vehicle (PBS) or normal goat IgG (10 ng; R & D Systems) was given to the control groups for leptin treatment or the neutralizing antibody, respectively.



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    antibodies against lepr biotin  (R&D Systems)
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    Fig. 2. <t>Leptin-R+</t> BMSCs develop senescence phenotype after HFD treatment. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) Cells were isolated from the femoral metaphyseal region, and the cell suspension was incubated <t>with</t> <t>antibodies</t> and subjected to flow cytometry analysis. n = 6. (A) Representative image of the flow cytometry analysis. The CD45-Leptin-R+ cell suspension was sorted via FACS and staining with Ki67 (green), p16 (green), and γH2AX (green) (n = 6). All these were co-staining with fibros actin (F-actin) (red) and DAPI (blue). Leptin-R+ cell suspension was subjected to EdU staining (red). (B) Representative images of staining of Ki67 (green), p16 (green), γH2AX (green), and EdU staining (red). (C–F) Quantification of Ki67 (%Ki67+ Cells) cells (green), p16(%p16+ Cells) cells (green), γH2AX (%γH2AX + Cells) cells (green) and EdU (%EdU+ Cells) cells staining (red). (G-H) The cell suspension prepared in (A) was subjected to FACS sorting followed by qPCR analysis. mRNA analysis of p16 (G)and p21(H) are shown. All data are shown as means ± standard deviations. *p < 0.05. Statistical significance was determined by unpaired, two-tailed Student's t-test.
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    Fig. 2. <t>Leptin-R+</t> BMSCs develop senescence phenotype after HFD treatment. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) Cells were isolated from the femoral metaphyseal region, and the cell suspension was incubated <t>with</t> <t>antibodies</t> and subjected to flow cytometry analysis. n = 6. (A) Representative image of the flow cytometry analysis. The CD45-Leptin-R+ cell suspension was sorted via FACS and staining with Ki67 (green), p16 (green), and γH2AX (green) (n = 6). All these were co-staining with fibros actin (F-actin) (red) and DAPI (blue). Leptin-R+ cell suspension was subjected to EdU staining (red). (B) Representative images of staining of Ki67 (green), p16 (green), γH2AX (green), and EdU staining (red). (C–F) Quantification of Ki67 (%Ki67+ Cells) cells (green), p16(%p16+ Cells) cells (green), γH2AX (%γH2AX + Cells) cells (green) and EdU (%EdU+ Cells) cells staining (red). (G-H) The cell suspension prepared in (A) was subjected to FACS sorting followed by qPCR analysis. mRNA analysis of p16 (G)and p21(H) are shown. All data are shown as means ± standard deviations. *p < 0.05. Statistical significance was determined by unpaired, two-tailed Student's t-test.
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    Fig. 2. <t>Leptin-R+</t> BMSCs develop senescence phenotype after HFD treatment. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) Cells were isolated from the femoral metaphyseal region, and the cell suspension was incubated <t>with</t> <t>antibodies</t> and subjected to flow cytometry analysis. n = 6. (A) Representative image of the flow cytometry analysis. The CD45-Leptin-R+ cell suspension was sorted via FACS and staining with Ki67 (green), p16 (green), and γH2AX (green) (n = 6). All these were co-staining with fibros actin (F-actin) (red) and DAPI (blue). Leptin-R+ cell suspension was subjected to EdU staining (red). (B) Representative images of staining of Ki67 (green), p16 (green), γH2AX (green), and EdU staining (red). (C–F) Quantification of Ki67 (%Ki67+ Cells) cells (green), p16(%p16+ Cells) cells (green), γH2AX (%γH2AX + Cells) cells (green) and EdU (%EdU+ Cells) cells staining (red). (G-H) The cell suspension prepared in (A) was subjected to FACS sorting followed by qPCR analysis. mRNA analysis of p16 (G)and p21(H) are shown. All data are shown as means ± standard deviations. *p < 0.05. Statistical significance was determined by unpaired, two-tailed Student's t-test.
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    Fig. 2. <t>Leptin-R+</t> BMSCs develop senescence phenotype after HFD treatment. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) Cells were isolated from the femoral metaphyseal region, and the cell suspension was incubated <t>with</t> <t>antibodies</t> and subjected to flow cytometry analysis. n = 6. (A) Representative image of the flow cytometry analysis. The CD45-Leptin-R+ cell suspension was sorted via FACS and staining with Ki67 (green), p16 (green), and γH2AX (green) (n = 6). All these were co-staining with fibros actin (F-actin) (red) and DAPI (blue). Leptin-R+ cell suspension was subjected to EdU staining (red). (B) Representative images of staining of Ki67 (green), p16 (green), γH2AX (green), and EdU staining (red). (C–F) Quantification of Ki67 (%Ki67+ Cells) cells (green), p16(%p16+ Cells) cells (green), γH2AX (%γH2AX + Cells) cells (green) and EdU (%EdU+ Cells) cells staining (red). (G-H) The cell suspension prepared in (A) was subjected to FACS sorting followed by qPCR analysis. mRNA analysis of p16 (G)and p21(H) are shown. All data are shown as means ± standard deviations. *p < 0.05. Statistical significance was determined by unpaired, two-tailed Student's t-test.
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    Fig. 2. <t>Leptin-R+</t> BMSCs develop senescence phenotype after HFD treatment. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) Cells were isolated from the femoral metaphyseal region, and the cell suspension was incubated <t>with</t> <t>antibodies</t> and subjected to flow cytometry analysis. n = 6. (A) Representative image of the flow cytometry analysis. The CD45-Leptin-R+ cell suspension was sorted via FACS and staining with Ki67 (green), p16 (green), and γH2AX (green) (n = 6). All these were co-staining with fibros actin (F-actin) (red) and DAPI (blue). Leptin-R+ cell suspension was subjected to EdU staining (red). (B) Representative images of staining of Ki67 (green), p16 (green), γH2AX (green), and EdU staining (red). (C–F) Quantification of Ki67 (%Ki67+ Cells) cells (green), p16(%p16+ Cells) cells (green), γH2AX (%γH2AX + Cells) cells (green) and EdU (%EdU+ Cells) cells staining (red). (G-H) The cell suspension prepared in (A) was subjected to FACS sorting followed by qPCR analysis. mRNA analysis of p16 (G)and p21(H) are shown. All data are shown as means ± standard deviations. *p < 0.05. Statistical significance was determined by unpaired, two-tailed Student's t-test.
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    (A) Representative immunofluorescence staining images of <t>leptin</t> receptor <t>(LepR,</t> red) in femurs from WT and Bmncr-KO mice. Nuclei, DAPI (blue). Scale bar: 100 μM. (B–C) Quantitative analysis of the number of LepR+ BMSCs in metaphysis and diaphysis regions of femurs (n = 5 per group). (D–E) FACS analysis dot plot (D) and quantitation of LepR+ BMSCs (E) (n = 5 per group). Data are mean ± SD. *P < 0.05 (Student’s t test).
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    Fig. 2. Leptin-R+ BMSCs develop senescence phenotype after HFD treatment. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) Cells were isolated from the femoral metaphyseal region, and the cell suspension was incubated with antibodies and subjected to flow cytometry analysis. n = 6. (A) Representative image of the flow cytometry analysis. The CD45-Leptin-R+ cell suspension was sorted via FACS and staining with Ki67 (green), p16 (green), and γH2AX (green) (n = 6). All these were co-staining with fibros actin (F-actin) (red) and DAPI (blue). Leptin-R+ cell suspension was subjected to EdU staining (red). (B) Representative images of staining of Ki67 (green), p16 (green), γH2AX (green), and EdU staining (red). (C–F) Quantification of Ki67 (%Ki67+ Cells) cells (green), p16(%p16+ Cells) cells (green), γH2AX (%γH2AX + Cells) cells (green) and EdU (%EdU+ Cells) cells staining (red). (G-H) The cell suspension prepared in (A) was subjected to FACS sorting followed by qPCR analysis. mRNA analysis of p16 (G)and p21(H) are shown. All data are shown as means ± standard deviations. *p < 0.05. Statistical significance was determined by unpaired, two-tailed Student's t-test.

    Journal: Cellular signalling

    Article Title: Uptake of ox-LDL by binding to LRP6 mediates oxidative stress-induced BMSCs senescence promoting obesity-related bone loss.

    doi: 10.1016/j.cellsig.2024.111114

    Figure Lengend Snippet: Fig. 2. Leptin-R+ BMSCs develop senescence phenotype after HFD treatment. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.) Cells were isolated from the femoral metaphyseal region, and the cell suspension was incubated with antibodies and subjected to flow cytometry analysis. n = 6. (A) Representative image of the flow cytometry analysis. The CD45-Leptin-R+ cell suspension was sorted via FACS and staining with Ki67 (green), p16 (green), and γH2AX (green) (n = 6). All these were co-staining with fibros actin (F-actin) (red) and DAPI (blue). Leptin-R+ cell suspension was subjected to EdU staining (red). (B) Representative images of staining of Ki67 (green), p16 (green), γH2AX (green), and EdU staining (red). (C–F) Quantification of Ki67 (%Ki67+ Cells) cells (green), p16(%p16+ Cells) cells (green), γH2AX (%γH2AX + Cells) cells (green) and EdU (%EdU+ Cells) cells staining (red). (G-H) The cell suspension prepared in (A) was subjected to FACS sorting followed by qPCR analysis. mRNA analysis of p16 (G)and p21(H) are shown. All data are shown as means ± standard deviations. *p < 0.05. Statistical significance was determined by unpaired, two-tailed Student's t-test.

    Article Snippet: For flow cytometric analysis of LepR cells, antibodies against mouse leptin receptor (R&D Systems, AF497, 1:500) was used.

    Techniques: Isolation, Suspension, Incubation, Flow Cytometry, Staining, Two Tailed Test

    (A) Representative immunofluorescence staining images of leptin receptor (LepR, red) in femurs from WT and Bmncr-KO mice. Nuclei, DAPI (blue). Scale bar: 100 μM. (B–C) Quantitative analysis of the number of LepR+ BMSCs in metaphysis and diaphysis regions of femurs (n = 5 per group). (D–E) FACS analysis dot plot (D) and quantitation of LepR+ BMSCs (E) (n = 5 per group). Data are mean ± SD. *P < 0.05 (Student’s t test).

    Journal: The Journal of Clinical Investigation

    Article Title: Long noncoding RNA Bmncr regulates mesenchymal stem cell fate during skeletal aging

    doi: 10.1172/JCI99044

    Figure Lengend Snippet: (A) Representative immunofluorescence staining images of leptin receptor (LepR, red) in femurs from WT and Bmncr-KO mice. Nuclei, DAPI (blue). Scale bar: 100 μM. (B–C) Quantitative analysis of the number of LepR+ BMSCs in metaphysis and diaphysis regions of femurs (n = 5 per group). (D–E) FACS analysis dot plot (D) and quantitation of LepR+ BMSCs (E) (n = 5 per group). Data are mean ± SD. *P < 0.05 (Student’s t test).

    Article Snippet: For immunofluorescence staining, we incubated the sections with primary antibodies against leptin receptor (R&D Systems, BAF497), osteocalcin (Takara, M173), SP7 (Abcam, ab22552), perilipin (Abcam, ab172907), and GFP (Rockland, 600-101-215).

    Techniques: Immunofluorescence, Staining, Quantitation Assay