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Image Search Results
Journal: Development (Cambridge, England)
Article Title: HB-EGF promotes epithelial cell migration in eyelid development.
doi: 10.1242/dev.02030
Figure Lengend Snippet: Fig. 5. sHB-EGF activates EGFR-ERK signaling but not JNK signaling in the extending leading edge. (A,B) lacZ expression at the tip of the leading edge of HBdel/+ (A) and HBdel/del (B) eyelids. (C,D) Detection of sHB-EGF protein in the leading edge of HBdel/+ (C) and HBdel/del (D) eyelids. (E,F) High-magnification views of boxed areas in C and D. (G-N) State of activation of EGFR and downstream signaling molecules in the leading edge of HBdel/+ (G,I,K,M) and HBdel/del (H,J,L,N) eyelids. (G,H) Phosphorylated EGFR. (I,J) Total EGFR protein. (K,L) Phosphorylated ERK. (M,N) Phosphorylated JNK. Scale bars: 100 m for A-D,G-N; 20 m for E,F.
Article Snippet:
Techniques: Expressing, Activation Assay
Journal: Development (Cambridge, England)
Article Title: HB-EGF promotes epithelial cell migration in eyelid development.
doi: 10.1242/dev.02030
Figure Lengend Snippet: Fig. 6. EGFR contributes to HB-EGF-dependent eyelid closure process. (A,B) Neonatal eyelid of a wild-type (A) and a double mutant mouse carrying the HB-EGF null allele and the waved 2 EGFR allele, showing an EOB phenotype (B). (C) Penetrance of the EOB phenotype in compound mutants carrying the HB-EGF null (‘d’) and waved 2 (‘wa2’) alleles. Blue bars indicate pups with normal closed eyes; red bars indicate pups with EOB.
Article Snippet:
Techniques: Mutagenesis
Journal: Development (Cambridge, England)
Article Title: HB-EGF promotes epithelial cell migration in eyelid development.
doi: 10.1242/dev.02030
Figure Lengend Snippet: Fig. 8. Proposed model for the function of HB- EGF in leading edge formation during eyelid closure. (A) Before E15.0, the leading edge is still not formed, and HB-EGF expression is not detectable. (B) At E15.0, the leading edge starts to extend, and HB-EGF expression appears at the tip of the leading edge. (C) From E15.0 to E16.0, HB-EGF is constitutively expressed at the tip of the extending leading edge. On the surface of the cells located in this region, ectodomain shedding of proHB-EGF may be mediated by ADAM17 (TACE), allowing sHB-EGF to diffuse throughout the leading edge region. sHB-EGF binds to and activates EGFR and the ERK pathway, resulting in F-actin polymerization and promotion of epithelial sheet migration.
Article Snippet:
Techniques: Expressing, Migration
Journal: Oncotarget
Article Title: Antibody neutralization of cell-surface gC1qR/HABP1/SF2-p32 prevents lamellipodia formation and tumorigenesis
doi: 10.18632/oncotarget.10267
Figure Lengend Snippet: A-D. A549 cells were serum-starved for 18 h and pretreated with 10 μg/mL of mock IgG or mAb 3D9 for 4 h and stimulated for 10 min by FBS (10%) (A), EGF (50 ng/mL) (B), IGF-1 (100 ng/mL) (C) and PDGF (20 ng/mL) (D) for 10 min. H-J. MDA-MB-231 cells were serum-starved for 18 h and pretreated with 10 μg/mL of mock IgG or mAb 3D9 for 4 h and stimulated for 10 min by FBS (10%) (H), EGF (50 ng/mL) (I) and IGF-1 (100 ng/mL) (J). Phosphorylated and total forms of Akt, Erk1/2, EGFR, IGFR and PDGFR were analyzed by immunoblotting using GAPDH as a loading control. The ratio of p-Akt/Akt E and K. , p-Erk/Erk F and L. , p-EGFR/EGFR G and M. , p-IGFR/IGFR (G and M) and p-PDGFR/PDGFR (G) was calculated from the band intensities for p-Akt, Akt, p-Erk1/2, Erk1/2, p-EGFR, EGFR, p-IGFR, IGFR, p-PDGFR and PDGFR in the immunoblottings (A-D and H-J).
Article Snippet: Anti-phospho-Akt, FAK, phospho-FAK, phospho-IGFR, VEGF, phospho-VEGF, phospho-PDGF, PDGF and PDH antibodies were purchased from
Techniques: Western Blot