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fak inhibitor  (MedChemExpress)


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    MedChemExpress fak inhibitor
    Fak Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 53 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fak inhibitor/product/MedChemExpress
    Average 95 stars, based on 53 article reviews
    fak inhibitor - by Bioz Stars, 2026-02
    95/100 stars

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    Selleck Chemicals fak inhibitor
    Fig. 4 Osteoblast differentiation-associated differentially expressed genes <t>after</t> <t>LIPUS</t> treatment. (A) Fold changes in the expression of upregulated genes associated with the term “osteoblast differentiation” in BMSCs after LIPUS treatment. (B) Random forest analysis revealed that ITGA11 had the highest mean decrease Gini coefficient and played a key role in regulating the biological process of “osteoblast differentiation”. (C) Protein-protein interac tion analysis of ITGA11-related proteins revealed that ITGA11 is closely related to the extracellular matrix, integrin and focal adhesion signals. (D) Focal adhesion signalling pathway diagram showing that extracellular matrix binding to integrins can regulate osteoblast differentiation by activating <t>FAK</t> phosphorylation
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    Fig. 4 Osteoblast differentiation-associated differentially expressed genes after LIPUS treatment. (A) Fold changes in the expression of upregulated genes associated with the term “osteoblast differentiation” in BMSCs after LIPUS treatment. (B) Random forest analysis revealed that ITGA11 had the highest mean decrease Gini coefficient and played a key role in regulating the biological process of “osteoblast differentiation”. (C) Protein-protein interac tion analysis of ITGA11-related proteins revealed that ITGA11 is closely related to the extracellular matrix, integrin and focal adhesion signals. (D) Focal adhesion signalling pathway diagram showing that extracellular matrix binding to integrins can regulate osteoblast differentiation by activating FAK phosphorylation

    Journal: BMC oral health

    Article Title: LIPUS promotes osteogenic differentiation of rat BMSCs and osseointegration of dental implants by regulating ITGA11 and focal adhesion pathway.

    doi: 10.1186/s12903-024-05411-2

    Figure Lengend Snippet: Fig. 4 Osteoblast differentiation-associated differentially expressed genes after LIPUS treatment. (A) Fold changes in the expression of upregulated genes associated with the term “osteoblast differentiation” in BMSCs after LIPUS treatment. (B) Random forest analysis revealed that ITGA11 had the highest mean decrease Gini coefficient and played a key role in regulating the biological process of “osteoblast differentiation”. (C) Protein-protein interac tion analysis of ITGA11-related proteins revealed that ITGA11 is closely related to the extracellular matrix, integrin and focal adhesion signals. (D) Focal adhesion signalling pathway diagram showing that extracellular matrix binding to integrins can regulate osteoblast differentiation by activating FAK phosphorylation

    Article Snippet: In the LIPUS experiment, 5 μM FAK inhibitor (PF573228, Selleck, Houston, USA) was used to inhibit FAK phosphorylation.

    Techniques: Expressing, Binding Assay, Phospho-proteomics

    Fig. 6 LIPUS promoted the osteogenic differentiation of BMSCs by upregulating ITGA11. (A, B) Three groups of ITGA11 knockdown lentiviruses exhib ited good knockdown efficiency in rat BMSCs. The original blots are presented in Supplementary Figure S5. (C) LIPUS induced FAK phosphorylation by upregulating ITGA11. The original blots are presented in Supplementary Figure S6. (D) ALP and alizarin red staining revealed that LIPUS promoted the osteogenic differentiation of rat BMSCs by upregulating ITGA11. (E) LIPUS increased ALP activity in BMSCs by upregulating ITGA11. (F) LIPUS promoted matrix mineralization in BMSCs by upregulating ITGA11. The data are presented as the mean ± standard deviation; *p < 0.05; ** p < 0.01

    Journal: BMC oral health

    Article Title: LIPUS promotes osteogenic differentiation of rat BMSCs and osseointegration of dental implants by regulating ITGA11 and focal adhesion pathway.

    doi: 10.1186/s12903-024-05411-2

    Figure Lengend Snippet: Fig. 6 LIPUS promoted the osteogenic differentiation of BMSCs by upregulating ITGA11. (A, B) Three groups of ITGA11 knockdown lentiviruses exhib ited good knockdown efficiency in rat BMSCs. The original blots are presented in Supplementary Figure S5. (C) LIPUS induced FAK phosphorylation by upregulating ITGA11. The original blots are presented in Supplementary Figure S6. (D) ALP and alizarin red staining revealed that LIPUS promoted the osteogenic differentiation of rat BMSCs by upregulating ITGA11. (E) LIPUS increased ALP activity in BMSCs by upregulating ITGA11. (F) LIPUS promoted matrix mineralization in BMSCs by upregulating ITGA11. The data are presented as the mean ± standard deviation; *p < 0.05; ** p < 0.01

    Article Snippet: In the LIPUS experiment, 5 μM FAK inhibitor (PF573228, Selleck, Houston, USA) was used to inhibit FAK phosphorylation.

    Techniques: Knockdown, Phospho-proteomics, Staining, Activity Assay, Standard Deviation

    Fig. 7 LIPUS promoted osteogenic gene expression in BMSCs by activating focal adhesion pathway downstream of ITGA11. (A) LIPUS increased ITGA11 expression and activated the downstream focal adhesion pathway. The original blots are presented in Supplementary Figure S7. (B-D) LIPUS promoted COL1A1, OCN, and BSP mRNA expression by activating the focal adhesion pathway. (E) Pathway diagram showing that LIPUS can promote the osteogenic differentiation of rat BMSCs by regulating the ITGA11-FAK/PI3K/AKT/GSK3β/β-catenin signalling pathway. The data are presented as the mean ± standard deviation; *p < 0.05; ** p < 0.01

    Journal: BMC oral health

    Article Title: LIPUS promotes osteogenic differentiation of rat BMSCs and osseointegration of dental implants by regulating ITGA11 and focal adhesion pathway.

    doi: 10.1186/s12903-024-05411-2

    Figure Lengend Snippet: Fig. 7 LIPUS promoted osteogenic gene expression in BMSCs by activating focal adhesion pathway downstream of ITGA11. (A) LIPUS increased ITGA11 expression and activated the downstream focal adhesion pathway. The original blots are presented in Supplementary Figure S7. (B-D) LIPUS promoted COL1A1, OCN, and BSP mRNA expression by activating the focal adhesion pathway. (E) Pathway diagram showing that LIPUS can promote the osteogenic differentiation of rat BMSCs by regulating the ITGA11-FAK/PI3K/AKT/GSK3β/β-catenin signalling pathway. The data are presented as the mean ± standard deviation; *p < 0.05; ** p < 0.01

    Article Snippet: In the LIPUS experiment, 5 μM FAK inhibitor (PF573228, Selleck, Houston, USA) was used to inhibit FAK phosphorylation.

    Techniques: Gene Expression, Expressing, Standard Deviation