primary antibody for p-cjun  (Cell Signaling Technology Inc)

Journal: PLoS ONE

Article Title: Activin B Promotes Epithelial Wound Healing In Vivo through RhoA-JNK Signaling Pathway

doi: 10.1371/journal.pone.0025143

Figure Lengend Snippet: Twelve mice were randomly assigned to PBS group and Act B group (n = 6). Immunohistochemistry indicated increased numbers of p-JNK-positive (A) and p-cJun-positive cells (C) at the wounded skin on day 3 and day 5 after activin B treatment, as compared with PBS control. Enlarged images of the boxed area were presented on the right side. Scale bars: 100 µm. Quantified percentages of p-JNK and p-cJun immunopositive cells are presented in (B) and (D) respectively. (E, F) Western blotting showed the level of JNK phosphorylation reached the highest value on day 3 and higher than PBS group on day 1 to day 5. 3 h, 6 h, 12 h: 3, 6 and 12 hours after wound. * P <0.05, ** P <0.01, compared with PBS control.

Article Snippet: Primary antibodies for rabbit polyclonal p-cJun, p-ERK and p-p38 were purchased from Cell Signaling Technology (Boston, MA).

Techniques: Immunohistochemistry, Control, Western Blot, Phospho-proteomics

Journal: PLoS ONE

Article Title: Activin B Promotes Epithelial Wound Healing In Vivo through RhoA-JNK Signaling Pathway

doi: 10.1371/journal.pone.0025143

Figure Lengend Snippet: Twenty four mice were randomly assigned to four groups: Act B+EGFP (n = 6), Act B+RhoAL63 (n = 6), Act B+RhoAN19 (n = 6) and Act B+Y27632 (n = 6). (A) Mice were treated with empty lentivirus vector (Act B+EGFP), constitutively active RhoA (L63) (Act B+RhoAL63), dominant negative RhoA (N19) (Act B+RhoAN19) or Act B+Y27632 after wound creation. Immunohistochemical staining for p-JNK (A) or p-cJun (C) was performed on indicated day after treatment. Pictures were taken at 100× magnification, and corresponding magnification pictures were taken at 400× magnification, Scale bars: 100 µm. The percentage of p-JNK-positive (B) or p-cJun-positive (D) cells was quantified. * P <0.05 compared with PBS control. ** P <0.05 compared with PBS, Act B+RhoAN19, and Act B+Y27632 groups. *** P <0.05 compared with PBS, Act B, Act B+EGFP, Act B+RhoAN19, and Act B+Y27632 groups.

Article Snippet: Primary antibodies for rabbit polyclonal p-cJun, p-ERK and p-p38 were purchased from Cell Signaling Technology (Boston, MA).

Techniques: Plasmid Preparation, Dominant Negative Mutation, Immunohistochemical staining, Staining, Control

Journal: PLoS ONE

Article Title: Activin B Promotes Epithelial Wound Healing In Vivo through RhoA-JNK Signaling Pathway

doi: 10.1371/journal.pone.0025143

Figure Lengend Snippet: Twenty seven mice were randomly assigned to two groups: Act B+SP600125 (n = 16) and SP600125 (n = 11). For JNK inhibition, 0.2 ml SP600125 (5 µM) applied to the wound surface 30 min prior to 0.2 ml of activin B (10 ng/ml) administration, or SP600125 alone. Mice received SP600125 and activin B treatment three times a day. Immunohistochemical staining for p-JNK and p-cJun showed that JNK inhibitor suppressed the expressions of phosphorylated (activated) JNK (A, B) and cJun (C, D) after activin B administration. (E) SP600125 suppressed wound closure induced by activin B and delayed wound healing. (F) Wound closure rate was calculated 3 and 5 days after treatment. (G) BrdU-positive cells were visualized on both epithelium (i) and hair follicle (ii). Pictures were taken at 100× magnification, and corresponding magnification pictures were taken at 400× magnification. Scale bars: 100 µm. Data were quantified in three independent experiments and the number of BrdU-positive cells per mm 2 in epithelium (H) and hair follicle (I) was presented. * P <0.05 compared with PBS control. ** P <0.05 compared with PBS, Act B+SP600125 and/or SP600125 groups.

Article Snippet: Primary antibodies for rabbit polyclonal p-cJun, p-ERK and p-p38 were purchased from Cell Signaling Technology (Boston, MA).

Techniques: Inhibition, Immunohistochemical staining, Staining, Control

Journal: PLoS ONE

Article Title: Activin B Promotes Epithelial Wound Healing In Vivo through RhoA-JNK Signaling Pathway

doi: 10.1371/journal.pone.0025143

Figure Lengend Snippet: Twenty six mice were randomly assigned to two groups: Act B+Follistatin (n = 13) and Follistatin (n = 13). Mice were administered follistatin (0.2 ml 10 ng/ml), thirty minutes after activin B (0.2 ml 10 ng/ml) was administrated, or not. (A) Follistatin suppressed wound closure in mice treated with activin B. (B) Wound closure rate was calculated 3 and 5 days after treatment. Compared with Act B group, follistatin remarkably suppressed the Act B-induced wound healing process. Immunohistochemical staining for p-JNK and p-cJun showed that follistatin suppressed the expression of phosphorylated (activated) JNK (C, D) and cJun (E, F), compared with Act B group. Pictures were taken at 100× magnification, and corresponding magnification pictures were taken at 400× magnification. Scale bars: 100 µm. * P <0.05 compared with PBS control.

Article Snippet: Primary antibodies for rabbit polyclonal p-cJun, p-ERK and p-p38 were purchased from Cell Signaling Technology (Boston, MA).

Techniques: Immunohistochemical staining, Staining, Expressing, Control