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s6k  (Bioss)


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    Bioss s6k
    OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and <t>S6K</t> in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.
    S6k, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/s6k/product/Bioss
    Average 94 stars, based on 2 article reviews
    s6k - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Osteoclast-derived apoptotic bodies accelerate the pathological progression of osteoarthritis via disturbing subchondral bone remodeling"

    Article Title: Osteoclast-derived apoptotic bodies accelerate the pathological progression of osteoarthritis via disturbing subchondral bone remodeling

    Journal: Journal of Orthopaedic Translation

    doi: 10.1016/j.jot.2025.01.004

    OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and S6K in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.
    Figure Legend Snippet: OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and S6K in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.

    Techniques Used: Microscopy, Staining, Control, Marker, Western Blot, Expressing, Activation Assay



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    s6k  (Bioss)
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    Bioss s6k
    OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and <t>S6K</t> in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.
    S6k, 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
    https://www.bioz.com/result/s6k/product/Bioss
    Average 94 stars, based on 1 article reviews
    s6k - by Bioz Stars, 2026-02
    94/100 stars
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    p s6k  (Bioss)
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    OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and <t>S6K</t> in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.
    P S6k, 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
    https://www.bioz.com/result/p s6k/product/Bioss
    Average 94 stars, based on 1 article reviews
    p s6k - by Bioz Stars, 2026-02
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and S6K in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.

    Journal: Journal of Orthopaedic Translation

    Article Title: Osteoclast-derived apoptotic bodies accelerate the pathological progression of osteoarthritis via disturbing subchondral bone remodeling

    doi: 10.1016/j.jot.2025.01.004

    Figure Lengend Snippet: OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and S6K in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.

    Article Snippet: Antibodies againstp-PI3K (BS-5570R), PI3K (BS-4160R), p-AKT (BS-2849R), Akt (BS-0115R), p-S6K (BS-5671R), S6K (BS-1426R), Runx2(BS-1134R), β-Actin (BS-0061R), Gapdh (BS-2188R), β-tubulin (BS-0715R) were purchased from BIOSS Antibodies (Beijing, China).

    Techniques: Microscopy, Staining, Control, Marker, Western Blot, Expressing, Activation Assay

    OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and S6K in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.

    Journal: Journal of Orthopaedic Translation

    Article Title: Osteoclast-derived apoptotic bodies accelerate the pathological progression of osteoarthritis via disturbing subchondral bone remodeling

    doi: 10.1016/j.jot.2025.01.004

    Figure Lengend Snippet: OC-ABs promote osteogenesis of MSCs via RANKL reverse signaling pathway. ( A ) Schematic representation of the generation of OC-ABs from bone marrow macrophages (BMMs) through osteoclastogenesis followed by apoptotic induction and collection. ( B ) Fluorescent microscopy images of Annexin V staining confirming the apoptotic status of OC-ABs with and without STS treatment. ( C ) Upper panels: Representative images of ALP staining in MSCs treated with vehicle, control, OC-ABs, rapamycin, and soluble sRANKL. Lower panels: Alizarin Red staining demonstrating calcium deposition as a marker of mineralization in the same treatment groups. ( D ) Western blot analysis showing phosphorylated and total forms of PI3K, Akt, and S6K in MSCs treated with OC-ABs, sRANKL, rapamycin, and vehicle (control). RUNX2 protein expression is also presented, with β-actin and GAPDH as loading controls. ( E ) Densitometric quantification of phosphorylated PI3K, Akt, and S6K normalized to their total forms, indicating increased activation in OC-AB treated cells. ( F ) Relative expression levels of osteogenic genes ALP , RUNX2 , and COL1A1 measured by qPCR. ( G ) Quantification of ALP and Alizarin Red staining. ∗∗ p < 0.01, ∗ p < 0.05.

    Article Snippet: Antibodies againstp-PI3K (BS-5570R), PI3K (BS-4160R), p-AKT (BS-2849R), Akt (BS-0115R), p-S6K (BS-5671R), S6K (BS-1426R), Runx2(BS-1134R), β-Actin (BS-0061R), Gapdh (BS-2188R), β-tubulin (BS-0715R) were purchased from BIOSS Antibodies (Beijing, China).

    Techniques: Microscopy, Staining, Control, Marker, Western Blot, Expressing, Activation Assay