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1.
Figure 2

Figure 2. From: STAT3 SIGNALING IS INDUCED BY INTERCELLULAR ADHESION IN SQUAMOUS CELL CARCINOMA CELLS.

Induction of STAT3-Y705 activation by cell-cell adhesion. Cell monolayer cultures of (A) HaCaT, (B) HSC-2, (C) UMSCC10A and (D) LMF4 were processed for Ca2+-switch assay as in and cell lysates were analyzed for STAT3-Y705 and total STAT3 by immunoblotting.

Akiko Onishi, et al. Exp Cell Res. ;314(2):377-386.
2.
Figure 3

Figure 3. From: STAT3 SIGNALING IS INDUCED BY INTERCELLULAR ADHESION IN SQUAMOUS CELL CARCINOMA CELLS.

Intercellular adhesion mediated phosphorylation of STAT1-Y701 and STAT3-S727 in HSC-3 cells. Cultures of HSC-3 cells were processed as in for calcium switch assay (A) or for MCA (B). As a positive control, serum-starved cells were stimulated with 15 ng/ml EGF for 30 min (A). Cell lysates were prepared and analyzed by immunoblotting as indicated for pSTAT-Y701 or pSTAT-S727.

Akiko Onishi, et al. Exp Cell Res. ;314(2):377-386.
3.
Figure 6

Figure 6. From: STAT3 SIGNALING IS INDUCED BY INTERCELLULAR ADHESION IN SQUAMOUS CELL CARCINOMA CELLS.

Localization of phosphorylated STAT3-Y705 in cell aggregates. (A) HSC-3 cells were grown as MCA on poly-HEMA coated plates. For each time point MCA were harvested and collected on poly-L-lysine coated coverslips, fixed, permeabilized and stained with antibodies to pSTAT-Y705. (B) pSTAT3-Y705 was visualized by confocal microscopy in MCA after 6 and 12 h of culture. Note: for clarity, the nuclear DAPI stain is presented in red for contrast with the FITC-conjugated pSTAT3-Y703 staining. Bar, 20 μm.

Akiko Onishi, et al. Exp Cell Res. ;314(2):377-386.
4.
Figure 5

Figure 5. From: STAT3 SIGNALING IS INDUCED BY INTERCELLULAR ADHESION IN SQUAMOUS CELL CARCINOMA CELLS.

Localization of phosphorylated STAT3-Y705 during Ca2+-induced cell-cell contact. Immunofluorescence analysis of HSC-3 cells cultured to 100% confluence and subjected to Ca+2 switch assay. Cells were either left untreated or treated with EGTA for 45 min and then exposed to Ca+2-containing media for 60 min. Cells were then fixed, permeabilized and processed for immunostaining with antibodies to E-cadherin (red) and phosphorylated STAT3-Y705 (green); DAPI was used to stain nuclei (blue). Magnified images of the cell are indicated by the dashed boxes. Arrow indicates junctional localization of E-cadherin and phospho-STAT3-Y705. Bars, 20 μm; 5μm

Akiko Onishi, et al. Exp Cell Res. ;314(2):377-386.
5.
Figure 1

Figure 1. From: STAT3 SIGNALING IS INDUCED BY INTERCELLULAR ADHESION IN SQUAMOUS CELL CARCINOMA CELLS.

Cell-cell interactions induce STAT3-Y705 phosphorylation. (A) Confluent HSC-3 monolayer cells were starved overnight and processed for Ca2+-switch assay as described in Methods and Materials. Cell lysates were then analyzed by immunoblotting for phosphorylated STAT3-Y705 and total STAT3 as indicated. (B) HSC-3 cells cultured as above were harvested and processed for centrifugal cell packing. Cells were incubated at 37°C as cell pellets or left as a single cell suspension for the indicated times. Cell lysates were prepared and analyzed for phosphorylated STAT3-Y705 by immunoblotting. (C) HSC-3 cells were cultured as single cells (SC) or as multicellular aggregates (MCA) (see Materials and Methods) for the indicated times. Cell lysates were prepared and immunoblotted for phosphorylated-STAT3-Y705. As a control serum-starved monolayer cells were treated with EGF (15 ng/ml) for 30 min.

Akiko Onishi, et al. Exp Cell Res. ;314(2):377-386.
6.
Figure 7

Figure 7. From: STAT3 SIGNALING IS INDUCED BY INTERCELLULAR ADHESION IN SQUAMOUS CELL CARCINOMA CELLS.

Inhibition of cell-cell contact by function-blocking E-cadherin antibody inhibits STAT3 phosphorylation. (A) Serum-starved confluent HSC-3 cells were processed for Ca2+-switch assay in presence of control IgG or function blocking E-cadherin antibody (She78-7) for 30 or 60 min. Cell lysates were prepared and analyzed for phosphorylated STAT3-Y705 and total STAT3. (B) HSC-3 cells were detached non-enzymatically, permitted to form MCAs in the presence of 5 μg/ml E-cadherin functional blocking antibody or control isotype IgG. Phase-contrast microphotographs of cells after 6 h of MCA culture. Bar, 20 μm. (C) Corresponding STAT3 phosphorylation status is shown as assessed by immunoblotting with anti-pSTAT antibody of the cell extracts. Results are representative of three independent experiments.

Akiko Onishi, et al. Exp Cell Res. ;314(2):377-386.
7.
Figure 4

Figure 4. From: STAT3 SIGNALING IS INDUCED BY INTERCELLULAR ADHESION IN SQUAMOUS CELL CARCINOMA CELLS.

Effect of inhibitors on intercellular adhesion mediated STAT3-Y705 phosphorylation. (A) Serum-starved monolayer HSC-3 cells were pretreated with inhibitors for epidermal growth factor (EGF) receptor (AG1478), Janus-activated kinase (AG490), and Src-family tyrosine kinase (SU6656), or DMSO vehicle alone for 1 h prior to and during performance of the calcium-switch assay. After calcium-induced cell-cell contact for 60 min, cell lysates were processed for immunoblotting with antibodies to pSTAT3-Y705 and total STAT3. (B) Serum-starved cells were processed as in (A) in the absence or presence of 1 and 10 μM AG1478 or DMSO alone for 60 min. Cell lysates were collected and analyzed for pSTAT3-Y705 and total STAT3 by immunoblotting. (C) Serum-starved HSC-3 cells were treated with 15 ng/ml of EGF in the absence or presence of 1 and 10 μM AG1478 or DMSO alone for 60 min. Cell lysates were collected and analyzed for pEGFR and pSTAT3-Y705 by immunoblotting. Membranes were stripped and reprobed for total EGFR and STAT3. (D) Serum-starved cells were processed as in (A) or in the presence of 1 μM PD168393. Cell lysates were collected and analyzed for pSTAT3-Y705 and total STAT3 by immunoblotting.

Akiko Onishi, et al. Exp Cell Res. ;314(2):377-386.

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