fgfr3 antibody Search Results


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Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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Novus Biologicals fgfr3 antibody
Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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R&D Systems fgfr
Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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R&D Systems cell surface marker fgfr3
Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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Figure 3. P68 RNA helicase transcriptionally <t>regulates</t> <t>PDGFR-β</t> expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and <t>FGFR</t> (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.
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Image Search Results


Figure 3. P68 RNA helicase transcriptionally regulates PDGFR-β expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and FGFR (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.

Journal: Journal of Cancer

Article Title: P68 RNA Helicase facilitates Breast Cancer progression by promoting Proliferation and Migration via PDGFR-β/AR axis.

doi: 10.7150/jca.61505

Figure Lengend Snippet: Figure 3. P68 RNA helicase transcriptionally regulates PDGFR-β expression in breast cancer cells. (A, B) Levels of p-PDGFRβ (IB: p-PDGFRβ) and pERK ½ (IB:pERK1/2), an established effector of PDGFR-β signaling in MDAMB231 (A) and BT549 (B) cells were analyzed by immunoblot upon PDGF-BB (20 ng/ml, 24h) stimulation. Levels of ERK ½ (IB:ERK1/2) and PDGFR-β (IB: PDGFRβ) are the loading controls. (C, D) Immunoblot analysis (C) of PDGFR-β (IB: PDGFR−β), EGFR (IB:EGFR), and FGFR (IB:FGFR) and their relative mRNA expression (D) in PDGF-BB stimulated MDAMB231 and BT549 cells upon p68 knockdown. Knockdown efficiency of p68 (IB:p68) was analyzed by immunoblot. Immunoblot of β-actin (IB:β-actin) is a loading control. (E) In vitro scratch wound healing assay of MDAMB231 cells transfected with p68 siRNA or co-transfected with p68 siRNA and PDGFRβ plasmid compared with control siRNA at 0 h and 24 h upon PDGF-BB stimulation. (F & G) Quantitative analyses of the migrating PDGF-BB stimulated MDAMB231 (F), and BT549 (G). The results represent findings of five independent experiments. Error bars represent mean ± S.E.M. **P<0.01, ****P<0.0001, ns denotes non-significant.

Article Snippet: The proteins were analyzed by immunoblotting probed with antibodies against p68 (SCBT, sc-126730), PDGFR-β (Abclonal, Ab2180), phospho-PDG FR-β (SCBT, Sc365465), phospho-EGFR (Abclonal, Ab 40815), EGFR (Cell signaling, 26465), FGFR (SCBT, sc-390423), N-Cadherin (Invitrogen, 33-3900), E-Cadherin (Biosciences, 610404), Vimentin (Protein tech, 60330), Snail (Abcam, 17732), AR (Agilent, M356201), β-Actin (2bscientific, R15006MC4) according to the vendor’s instructions.

Techniques: Expressing, Western Blot, Knockdown, Control, In Vitro, Wound Healing Assay, Transfection, Plasmid Preparation