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- Antigen structure
- References [2]
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- Other assay [2]
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- Product number
- PA1-86605 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- STAT3 Polyclonal Antibody
- Antibody type
- Polyclonal
- Antigen
- Synthetic peptide
- Description
- Predicted to react with rat based on sequence homology.
- Concentration
- 0.5 mg/mL
Submitted references Leptin reduces in vitro cementoblast mineralization and survival as well as induces PGE2 release by ERK1/2 commitment.
Adiponectin Interacts In-Vitro With Cementoblasts Influencing Cell Migration, Proliferation and Cementogenesis Partly Through the MAPK Signaling Pathway.
Ruiz-Heiland G, Yong JW, von Bremen J, Ruf S
Clinical oral investigations 2021 Apr;25(4):1933-1944
Clinical oral investigations 2021 Apr;25(4):1933-1944
Adiponectin Interacts In-Vitro With Cementoblasts Influencing Cell Migration, Proliferation and Cementogenesis Partly Through the MAPK Signaling Pathway.
Yong J, von Bremen J, Ruiz-Heiland G, Ruf S
Frontiers in pharmacology 2020;11:585346
Frontiers in pharmacology 2020;11:585346
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- Invitrogen Antibodies (provider)
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- Experimental details
- FIGURE 4 Adiponectin promotes JNK, ERK1/2 and P38 phosphorylation on OCCM-30 cells. (A,B) The expression of JNK (46 and 54 kDa), ERK1/2 (42 and 44 kDa) and P38 (42 kDa) expression as well as their phosphorylated forms after Adiponectin (20 ng/mL) stimulation were analyzed by Western Blots. beta-actin served as a loading control. Graphics show the relative expression of p-JNK, p-ERK1/2 and p-P38 compared to cells at time point 0 min. (C,D) Adiponectin (20 ng/mL) promotes STAT1 (98 KDa) and STAT3 (85 KDa) phosphorylation during a period of 30 min. Graphics show the relative expression of p-STAT1 and p-STAT3 compared to cells at time point 0 min. Values are expressed as means +- SD: Ns (not significant), * p < 0.05; ** p < 0.01; *** p < 0.001.
- Submitted by
- Invitrogen Antibodies (provider)
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- Experimental details
- Fig. 2 Kinetic analysis performed on OCCM-30 cells after stimulation with leptin. The expression of SHP2; COX2; p-STAT1; STAT1; p-STAT3; STAT3; p-ERK1/2; ERK1/2; p-P38; P38; p-JNK; and JNK were visualized by western blot: Leptin upregulates p-STAT1; p-STAT3; and p-ERK1/2 as well as COX2 on OCCM cells whereas no activation of P38 or JNK was observed. Each experiment was repeated three times
