fak inhibitor (faki, (1 µm) Search Results


fak inhibitor 14 faki  (Tocris)
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Tocris fak inhibitor 14 faki
Fak Inhibitor 14 Faki, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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n formyl met leu phe fmlf  (R&D Systems)
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R&D Systems n formyl met leu phe fmlf
N Formyl Met Leu Phe Fmlf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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fak inhibitor  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology fak inhibitor
Fak Inhibitor, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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faki pf573228  (Tocris)
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Tocris faki pf573228
Faki Pf573228, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pf573228  (Tocris)
90
Tocris pf573228
STAT3 inhibition mediates CNTF repression by FAK. A ) FAK inhibition reduces STAT3 phosphorylation on its inhibitory residue (s727) as shown in western blots <t>of</t> <t>C6</t> cells incubated for 4 hours. Total STAT3 antibodies were used as internal controls. B ) Pre-incubation with a STAT3 antagonist reduced the CNTF-inducing effects of FAK inhibitor in C6 cells. Thus, FAK represses CNTF by inhibiting STAT3. An AP1 transcription factor antagonist was without effect. Data are fold compared to control (not shown) and means +/−SEM. C ) STAT3 binds the CNTF promoter region of C6 cells as shown by ChIP analysis. STAT3 antibody immunoprecipitates (IP) CNTF promoter DNA as shown by the PCR amplification products of two promoter-specific primer sets. Normal rabbit IgG was used as control for non-specific binding. Histone H3 was a positive control. D ) Sequencing of the amplification products of the STAT3 immunoprecipitate gave the predicted DNA regions. Key: Consensus STAT3 binding sites ; : CNTF initiation site; CNTF1 primer set (FWD, REV) ; ; < > denote DNA regions excluded from this panel for presentation purposes. E ) IL-6 treatment of C6 cells for 15 minutes robustly increased phosphorylation of STAT3 at the Tyr-705 residue (y705) with modest increases after CNTF and LIF as shown by western blot. Ser-727 phosphorylation (s727) or total STAT3 (tSTAT3) was not affected. Similar results were seen at 4 hours. The blot is representative of 4 independent experiments. F ) IL-6 induced only an ~10% increase in CNTF mRNA expression in C6 cells after 4 hours and did not augment <t>FAKi-induced</t> CNTF expression (n = 3-4 each, p < 0.05). G ) FAK inhibition reduced phosphorylation of STAT3 (y705) in C6 cells most notably under IL-6 treated conditions. Antibodies against total STAT3 were used as internal controls for western blots. Results were repeatable in independent experiments.
Pf573228, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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coincubation with faki  (Tocris)
95
Tocris coincubation with faki
STAT3 inhibition mediates CNTF repression by FAK. A ) FAK inhibition reduces STAT3 phosphorylation on its inhibitory residue (s727) as shown in western blots <t>of</t> <t>C6</t> cells incubated for 4 hours. Total STAT3 antibodies were used as internal controls. B ) Pre-incubation with a STAT3 antagonist reduced the CNTF-inducing effects of FAK inhibitor in C6 cells. Thus, FAK represses CNTF by inhibiting STAT3. An AP1 transcription factor antagonist was without effect. Data are fold compared to control (not shown) and means +/−SEM. C ) STAT3 binds the CNTF promoter region of C6 cells as shown by ChIP analysis. STAT3 antibody immunoprecipitates (IP) CNTF promoter DNA as shown by the PCR amplification products of two promoter-specific primer sets. Normal rabbit IgG was used as control for non-specific binding. Histone H3 was a positive control. D ) Sequencing of the amplification products of the STAT3 immunoprecipitate gave the predicted DNA regions. Key: Consensus STAT3 binding sites ; : CNTF initiation site; CNTF1 primer set (FWD, REV) ; ; < > denote DNA regions excluded from this panel for presentation purposes. E ) IL-6 treatment of C6 cells for 15 minutes robustly increased phosphorylation of STAT3 at the Tyr-705 residue (y705) with modest increases after CNTF and LIF as shown by western blot. Ser-727 phosphorylation (s727) or total STAT3 (tSTAT3) was not affected. Similar results were seen at 4 hours. The blot is representative of 4 independent experiments. F ) IL-6 induced only an ~10% increase in CNTF mRNA expression in C6 cells after 4 hours and did not augment <t>FAKi-induced</t> CNTF expression (n = 3-4 each, p < 0.05). G ) FAK inhibition reduced phosphorylation of STAT3 (y705) in C6 cells most notably under IL-6 treated conditions. Antibodies against total STAT3 were used as internal controls for western blots. Results were repeatable in independent experiments.
Coincubation With Faki, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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fak inhibitor (faki, (1 µm)  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology fak inhibitor (faki, (1 µm)
STAT3 inhibition mediates CNTF repression by FAK. A ) FAK inhibition reduces STAT3 phosphorylation on its inhibitory residue (s727) as shown in western blots <t>of</t> <t>C6</t> cells incubated for 4 hours. Total STAT3 antibodies were used as internal controls. B ) Pre-incubation with a STAT3 antagonist reduced the CNTF-inducing effects of FAK inhibitor in C6 cells. Thus, FAK represses CNTF by inhibiting STAT3. An AP1 transcription factor antagonist was without effect. Data are fold compared to control (not shown) and means +/−SEM. C ) STAT3 binds the CNTF promoter region of C6 cells as shown by ChIP analysis. STAT3 antibody immunoprecipitates (IP) CNTF promoter DNA as shown by the PCR amplification products of two promoter-specific primer sets. Normal rabbit IgG was used as control for non-specific binding. Histone H3 was a positive control. D ) Sequencing of the amplification products of the STAT3 immunoprecipitate gave the predicted DNA regions. Key: Consensus STAT3 binding sites ; : CNTF initiation site; CNTF1 primer set (FWD, REV) ; ; < > denote DNA regions excluded from this panel for presentation purposes. E ) IL-6 treatment of C6 cells for 15 minutes robustly increased phosphorylation of STAT3 at the Tyr-705 residue (y705) with modest increases after CNTF and LIF as shown by western blot. Ser-727 phosphorylation (s727) or total STAT3 (tSTAT3) was not affected. Similar results were seen at 4 hours. The blot is representative of 4 independent experiments. F ) IL-6 induced only an ~10% increase in CNTF mRNA expression in C6 cells after 4 hours and did not augment <t>FAKi-induced</t> CNTF expression (n = 3-4 each, p < 0.05). G ) FAK inhibition reduced phosphorylation of STAT3 (y705) in C6 cells most notably under IL-6 treated conditions. Antibodies against total STAT3 were used as internal controls for western blots. Results were repeatable in independent experiments.
Fak Inhibitor (Faki, (1 µm), supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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fak inhibitor defactinib hydrochloride  (MedChemExpress)
95
MedChemExpress fak inhibitor defactinib hydrochloride
STAT3 inhibition mediates CNTF repression by FAK. A ) FAK inhibition reduces STAT3 phosphorylation on its inhibitory residue (s727) as shown in western blots <t>of</t> <t>C6</t> cells incubated for 4 hours. Total STAT3 antibodies were used as internal controls. B ) Pre-incubation with a STAT3 antagonist reduced the CNTF-inducing effects of FAK inhibitor in C6 cells. Thus, FAK represses CNTF by inhibiting STAT3. An AP1 transcription factor antagonist was without effect. Data are fold compared to control (not shown) and means +/−SEM. C ) STAT3 binds the CNTF promoter region of C6 cells as shown by ChIP analysis. STAT3 antibody immunoprecipitates (IP) CNTF promoter DNA as shown by the PCR amplification products of two promoter-specific primer sets. Normal rabbit IgG was used as control for non-specific binding. Histone H3 was a positive control. D ) Sequencing of the amplification products of the STAT3 immunoprecipitate gave the predicted DNA regions. Key: Consensus STAT3 binding sites ; : CNTF initiation site; CNTF1 primer set (FWD, REV) ; ; < > denote DNA regions excluded from this panel for presentation purposes. E ) IL-6 treatment of C6 cells for 15 minutes robustly increased phosphorylation of STAT3 at the Tyr-705 residue (y705) with modest increases after CNTF and LIF as shown by western blot. Ser-727 phosphorylation (s727) or total STAT3 (tSTAT3) was not affected. Similar results were seen at 4 hours. The blot is representative of 4 independent experiments. F ) IL-6 induced only an ~10% increase in CNTF mRNA expression in C6 cells after 4 hours and did not augment <t>FAKi-induced</t> CNTF expression (n = 3-4 each, p < 0.05). G ) FAK inhibition reduced phosphorylation of STAT3 (y705) in C6 cells most notably under IL-6 treated conditions. Antibodies against total STAT3 were used as internal controls for western blots. Results were repeatable in independent experiments.
Fak Inhibitor Defactinib Hydrochloride, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


STAT3 inhibition mediates CNTF repression by FAK. A ) FAK inhibition reduces STAT3 phosphorylation on its inhibitory residue (s727) as shown in western blots of C6 cells incubated for 4 hours. Total STAT3 antibodies were used as internal controls. B ) Pre-incubation with a STAT3 antagonist reduced the CNTF-inducing effects of FAK inhibitor in C6 cells. Thus, FAK represses CNTF by inhibiting STAT3. An AP1 transcription factor antagonist was without effect. Data are fold compared to control (not shown) and means +/−SEM. C ) STAT3 binds the CNTF promoter region of C6 cells as shown by ChIP analysis. STAT3 antibody immunoprecipitates (IP) CNTF promoter DNA as shown by the PCR amplification products of two promoter-specific primer sets. Normal rabbit IgG was used as control for non-specific binding. Histone H3 was a positive control. D ) Sequencing of the amplification products of the STAT3 immunoprecipitate gave the predicted DNA regions. Key: Consensus STAT3 binding sites ; : CNTF initiation site; CNTF1 primer set (FWD, REV) ; ; < > denote DNA regions excluded from this panel for presentation purposes. E ) IL-6 treatment of C6 cells for 15 minutes robustly increased phosphorylation of STAT3 at the Tyr-705 residue (y705) with modest increases after CNTF and LIF as shown by western blot. Ser-727 phosphorylation (s727) or total STAT3 (tSTAT3) was not affected. Similar results were seen at 4 hours. The blot is representative of 4 independent experiments. F ) IL-6 induced only an ~10% increase in CNTF mRNA expression in C6 cells after 4 hours and did not augment FAKi-induced CNTF expression (n = 3-4 each, p < 0.05). G ) FAK inhibition reduced phosphorylation of STAT3 (y705) in C6 cells most notably under IL-6 treated conditions. Antibodies against total STAT3 were used as internal controls for western blots. Results were repeatable in independent experiments.

Journal: Cell Communication and Signaling : CCS

Article Title: Inhibition of a novel specific neuroglial integrin signaling pathway increases STAT3-mediated CNTF expression

doi: 10.1186/1478-811X-11-35

Figure Lengend Snippet: STAT3 inhibition mediates CNTF repression by FAK. A ) FAK inhibition reduces STAT3 phosphorylation on its inhibitory residue (s727) as shown in western blots of C6 cells incubated for 4 hours. Total STAT3 antibodies were used as internal controls. B ) Pre-incubation with a STAT3 antagonist reduced the CNTF-inducing effects of FAK inhibitor in C6 cells. Thus, FAK represses CNTF by inhibiting STAT3. An AP1 transcription factor antagonist was without effect. Data are fold compared to control (not shown) and means +/−SEM. C ) STAT3 binds the CNTF promoter region of C6 cells as shown by ChIP analysis. STAT3 antibody immunoprecipitates (IP) CNTF promoter DNA as shown by the PCR amplification products of two promoter-specific primer sets. Normal rabbit IgG was used as control for non-specific binding. Histone H3 was a positive control. D ) Sequencing of the amplification products of the STAT3 immunoprecipitate gave the predicted DNA regions. Key: Consensus STAT3 binding sites ; : CNTF initiation site; CNTF1 primer set (FWD, REV) ; ; < > denote DNA regions excluded from this panel for presentation purposes. E ) IL-6 treatment of C6 cells for 15 minutes robustly increased phosphorylation of STAT3 at the Tyr-705 residue (y705) with modest increases after CNTF and LIF as shown by western blot. Ser-727 phosphorylation (s727) or total STAT3 (tSTAT3) was not affected. Similar results were seen at 4 hours. The blot is representative of 4 independent experiments. F ) IL-6 induced only an ~10% increase in CNTF mRNA expression in C6 cells after 4 hours and did not augment FAKi-induced CNTF expression (n = 3-4 each, p < 0.05). G ) FAK inhibition reduced phosphorylation of STAT3 (y705) in C6 cells most notably under IL-6 treated conditions. Antibodies against total STAT3 were used as internal controls for western blots. Results were repeatable in independent experiments.

Article Snippet: To block STAT3 activation, the selective small molecule inhibitor Stattic (10 μM; Tocris; [ ]) was incubated with C6 cells 1 hour before addition of FAKi (PF573228).

Techniques: Inhibition, Phospho-proteomics, Residue, Western Blot, Incubation, Control, Amplification, Binding Assay, Positive Control, Sequencing, Expressing