FAK Antibody - #AF6397

Fig. 4. Evaluation of therapeutic efficiency and pH-responsive property of cetuximab (Cet)/focal adhesion kinase (FAK) small interfering RNA (siFAK)@zeolitic imidazolate framework-8 (ZIF-8)@TU177 cell membrane (TCM) in vitro. (A, B) The messenger RNA (mRNA) (A) and protein (B) levels of FAK in TU177 cells treated with free siFAK and siFAK-loaded nanocomplexes. (C) FAK mRNA levels of FAK in TU177 cells before and after three generations. (D–F) Viability (D), apoptosis (E), and live/dead status (F) of TU177 cells cultured with free Cet, free siFAK, Cet@ZIF-8@TCM, siFAK@ZIF-8@TCM, and Cet/siFAK@ZIF-8@TCM at pH 6.5 and 7.4. ∗P < 0.05 and ∗∗P < 0.01. ns: no significance. GAPDH: glyceraldehyde-3-phosphate dehydrogenase; PEA: phycoerythrin-area; UL: upper left; UR: upper right; LL: lower left; LR: lower right; FITC: fluorescein isothiocyanate.

Figure 8 |Western blot analysis of key proteins in the focal adhesion pathway after DBT treatment for 6 days. (A, C) Representatives blot from 3 independent experiments. (B, D) Densitometric quantification. GAPDH was used as an internal control. Values are the mean ± SEM, where n = 3. (*p < 0.05 as compared to the control, LSD).

Fig. 3 FAK promotes the polarization of macrophages in the Treg-macrophage co-culture system through PI3K/AKT/JAK/STAT3 and p38/JNK/ERK signal pathway A, B The expression of the PI3K, p-PI3K, AKT, p-AKT, p-FAK, FAK, JAK2, STAT3, p-STAT3 and p38, p-p38/JNK, p-JNK/ERK1/2, p-ERK1/2 in Treg-macrophage co-culture system were observed by the western blot, n = 3 in each group. #P 

Figure 5. - KRT7 expression affects the integrin-β1-FAK signaling and TGF-β signaling pathways. (A and B) Expression of proliferation- and migration-associated genes (PCNA, MMP9 and TIMP-1) were evaluated using western blotting in HEY cells. (C and D) Western blotting of proteins involved in integrin-β1-FAK signaling pathway in the KRT7-overexpressing HEY cells. (E) Expression of MMPs after knockdown of KRT7 in OVCAR433 cells. (F and G) Expression of the TGF-β signaling pathway-related proteins was evaluated by western blotting in KRT7-overexpressing HEY cells and KRT7-knockdown OVCAR433 cells. All experiments were performed at least three times. Results are presented as the mean ± standard deviation. **P<0.01. FAK, focal adhesion kinase; PCNA, proliferating cell nuclear antigen; FN, fibronectin; TIMP-1, TIMP metallopeptidase inhibitor 1; p-, phosphorylated; MMP, matrix metalloproteinase; KRT7, keratin 7; sh, short hairpin RNA; NC, negative control.

Fig. 6. FOXF1 can affect the activation of FAK signal pathway by regulating the expression of MFAP4. (a) The network diagram shows the signal pathways positively related to the high expression of FOXF1 and MFAP4. Green indicates that the activation of signaling pathways is significantly correlated with the expression of FOXF1, and the blue indicates that the activation of signaling pathways is significantly correlated with the expression of MFAP4. The network diagram displays the three signal pathways that are most relevant to both FOXF1 and MFAP4 (Pathways in Cancer, Focal Adhesion, Purine Metabolism). (b) GSEA shows that the high expression of FOXF1 and MFAP4 is significantly associated with Focal Adhesion signal pathway. (c) ssGSEA indicates that both high expression of FOXF1 and MFAP4 is significantly associated with Focal Adhesion signal pathway. (d) Protein expression of FAK and p-FAK (Tyr397) with FOXF1 and MFAP4 expression are detected by Western Blot. The network diagram was generated from “Cytoscape” software (version 3.10.2, https://cytoscape.org/) and the GSEA plots were generated from the “ggplot2” (version 3.5.0, https://github.com/tidyverse/ggplot2) package in R.

Figure 7 High NIBAN1 expression correlates with highly enriched focal adhesion signaling in bladder cancer. A. Gene Set Enrichment Analysis of The Cancer Genome Atlas bladder cancer dataset revealed a highly enriched gene signature of focal adhesion pathway in NIBAN1-high bladder cancer. B. GEM-resistant cells T24GR exhibited highly activated FAK and its downstream SRC/AKT signaling compared to GEM-sensitive T24 and 5637 cells. β-Actin was used as a loading control. C. Differentially expressed genes in T24GR cells with or without NIBAN1 knockdown. D. Pathway enrichment analysis was conducted on downregulated genes (n = 173) using GO, KEGG, and Reactome Gene Sets annotations.