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Cell Signaling Technology Inc anti raf 1
TLN-4601 inhibits tumor growth and K-Ras signaling in vivo . MIA PaCa-2 xenograft-bearing nude mice were treated with TLN-4601 (30 mg/kg s.c., once a day Monday through Friday for three consecutive weeks) or gemcitabine (60 mg/kg i.p., twice a week for 4 weeks). Control group received 5 ml/kg of drug-free vehicle (15% PS80/5% PEG 400/5% EtOH/80% D5W) s.c., once a day Monday through Friday for three consecutive weeks. (A). Tumors were excised, lysed, and probed for <t>Raf-1</t> protein expression (B); horizontal lines mark the mean of n = 5 mice.
Anti Raf 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti raf 1/product/Cell Signaling Technology Inc
Average 90 stars, based on 1 article reviews
Price from $9.99 to $1999.99
anti raf 1 - by Bioz Stars, 2020-07
90/100 stars

Images

1) Product Images from "TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-ERK MAPK signaling"

Article Title: TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-ERK MAPK signaling

Journal: Journal of Molecular Signaling

doi: 10.1186/1750-2187-5-18

TLN-4601 inhibits tumor growth and K-Ras signaling in vivo . MIA PaCa-2 xenograft-bearing nude mice were treated with TLN-4601 (30 mg/kg s.c., once a day Monday through Friday for three consecutive weeks) or gemcitabine (60 mg/kg i.p., twice a week for 4 weeks). Control group received 5 ml/kg of drug-free vehicle (15% PS80/5% PEG 400/5% EtOH/80% D5W) s.c., once a day Monday through Friday for three consecutive weeks. (A). Tumors were excised, lysed, and probed for Raf-1 protein expression (B); horizontal lines mark the mean of n = 5 mice.
Figure Legend Snippet: TLN-4601 inhibits tumor growth and K-Ras signaling in vivo . MIA PaCa-2 xenograft-bearing nude mice were treated with TLN-4601 (30 mg/kg s.c., once a day Monday through Friday for three consecutive weeks) or gemcitabine (60 mg/kg i.p., twice a week for 4 weeks). Control group received 5 ml/kg of drug-free vehicle (15% PS80/5% PEG 400/5% EtOH/80% D5W) s.c., once a day Monday through Friday for three consecutive weeks. (A). Tumors were excised, lysed, and probed for Raf-1 protein expression (B); horizontal lines mark the mean of n = 5 mice.

Techniques Used: In Vivo, Mouse Assay, Expressing

TLN-4601 inhibits the K-Ras downstream signaling cascade in PDAC cells . Exponentially growing cells were treated with increasing concentrations of TLN-4601. After overnight exposure, cells were lysed and cellular extracts (30 μg protein) were separated on a 10% SDS-PAGE gel and transferred to nitrocellulose membranes. (A) Membranes were sequentially probed with Raf-1 and ERK1/2 (p44/42 MAP kinase) or (B) phospho-MEK1/2 (Ser217/221), MEK1 and vinculin (loading control). Blots are representatives of three independent experiments.
Figure Legend Snippet: TLN-4601 inhibits the K-Ras downstream signaling cascade in PDAC cells . Exponentially growing cells were treated with increasing concentrations of TLN-4601. After overnight exposure, cells were lysed and cellular extracts (30 μg protein) were separated on a 10% SDS-PAGE gel and transferred to nitrocellulose membranes. (A) Membranes were sequentially probed with Raf-1 and ERK1/2 (p44/42 MAP kinase) or (B) phospho-MEK1/2 (Ser217/221), MEK1 and vinculin (loading control). Blots are representatives of three independent experiments.

Techniques Used: SDS Page

2) Product Images from "Measles virus suppresses RIG-I-like receptor activation in dendritic cells via DC-SIGN-mediated inhibition of PP1 phosphatases"

Article Title: Measles virus suppresses RIG-I-like receptor activation in dendritic cells via DC-SIGN-mediated inhibition of PP1 phosphatases

Journal: Cell host & microbe

doi: 10.1016/j.chom.2014.06.008

Raf-1 activation via DC-SIGN decreases MV-induced type I IFN expression ( A,C,F,G ) IFN-β, MxA, and ISG15 mRNA expression by DCs 8 h after stimulation with poly(I:C)-LV and/or receptor crosslinking with isotype or DC-SIGN-specific antibodies ( A,C ) or 24 h after infection with rMV KS ( F,G ), in the absence or presence of Raf inhibitor GW5074 ( A,F ) or after Raf-1 silencing ( B,G ), measured by real-time PCR, normalized to GAPDH, and set at 1 in MV- or poly(I:C)-LV-stimulated (control-silenced) cells. Data are presented as mean ± SD. N.s., not statistically significant; *, P
Figure Legend Snippet: Raf-1 activation via DC-SIGN decreases MV-induced type I IFN expression ( A,C,F,G ) IFN-β, MxA, and ISG15 mRNA expression by DCs 8 h after stimulation with poly(I:C)-LV and/or receptor crosslinking with isotype or DC-SIGN-specific antibodies ( A,C ) or 24 h after infection with rMV KS ( F,G ), in the absence or presence of Raf inhibitor GW5074 ( A,F ) or after Raf-1 silencing ( B,G ), measured by real-time PCR, normalized to GAPDH, and set at 1 in MV- or poly(I:C)-LV-stimulated (control-silenced) cells. Data are presented as mean ± SD. N.s., not statistically significant; *, P

Techniques Used: Activation Assay, Expressing, Infection, Real-time Polymerase Chain Reaction

DC-SIGN-Raf-1 signaling inhibits dephosphorylation of RIG-I and Mda5 ( A–D ) RIG-I phosphorylation at Ser8 or Thr170 and Mda5 phosphorylation at Ser88 in DCs left unstimulated; or 3 h after stimulation by crosslinking with isotype or DC-SIGN-specific antibodies ( A,B ), in the absence or presence of Raf inhibitor GW5074 ( B ); or 8 or 16 h after rMV KS infection or 3 h after or rMV IC323 EGFP(1) in the absence or presence of Raf-1 inhibition via GW5074 ( C ) or Raf-1 silencing ( D ), as determined by flow cytometry. Data are representative of at least four ( A,B,C (rMV IC323 , 8 h rMV KS ), two ( C (16 h rMV KS )) or three ( D .
Figure Legend Snippet: DC-SIGN-Raf-1 signaling inhibits dephosphorylation of RIG-I and Mda5 ( A–D ) RIG-I phosphorylation at Ser8 or Thr170 and Mda5 phosphorylation at Ser88 in DCs left unstimulated; or 3 h after stimulation by crosslinking with isotype or DC-SIGN-specific antibodies ( A,B ), in the absence or presence of Raf inhibitor GW5074 ( B ); or 8 or 16 h after rMV KS infection or 3 h after or rMV IC323 EGFP(1) in the absence or presence of Raf-1 inhibition via GW5074 ( C ) or Raf-1 silencing ( D ), as determined by flow cytometry. Data are representative of at least four ( A,B,C (rMV IC323 , 8 h rMV KS ), two ( C (16 h rMV KS )) or three ( D .

Techniques Used: De-Phosphorylation Assay, Infection, Inhibition, Flow Cytometry, Cytometry

DC-SIGN-Raf-1 signaling inhibits RLR activation and type I IFN responses via phosphorylation of GADD34-PP1 inhibitor I-1 ( A,C ) Overall ( A ) or GADD34-specific ( C ) PP1 phosphatase activity in whole cell lysates of DCs 1 h after stimulation with poly(I:C)-LV and/or receptor crosslinking with isotype or DC-SIGN-specific antibodies (left panels) or 24 h after infection with rMV KS or rMV IC323 (right panels), in the absence or presence of Raf inhibitor GW5074. Data are presented as mean ± SD. ( B,E,F ) RIG-I phosphorylation at Ser8 or Thr170 and Mda5 phosphorylation at Ser88 in DCs left unstimulated; or 3 h after stimulation by receptor crosslinking with isotype or DC-SIGN-specific (antibodies ( B,F ); or 8 h after rMV KS infection ( E ), in the absence or presence of GADD34 inhibitor guanabenz (Gb) ( B ) or after GADD34 or I-1 silencing ( E,F ), as determined by flow cytometry. ( D ) I-1 phosphorylation at Ser or Thr residues, and association with PP1α or PP1γ after immunoprecipitation (IP) of I-1 from whole cell lysates of DCs left unstimulated or 3 h after infection with rMV KS , in the absence or presence of GW5074, determined by immunoblotting (IB). ( G,H ) IFN-β, MxA, and ISG15 mRNA expression by DCs 8 h after stimulation with poly(I:C)-LV and/or receptor crosslinking with isotype or DC-SIGN-specific antibodies ( G ) or 24 h after infection with rMV KS ( H ), after GADD34 or I-1 silencing, measured by real-time PCR, normalized to GAPDH, and set at 1 in MV- or poly(I:C)-LV-stimulated control-silenced cells. Data are presented as mean ± SD. *, P
Figure Legend Snippet: DC-SIGN-Raf-1 signaling inhibits RLR activation and type I IFN responses via phosphorylation of GADD34-PP1 inhibitor I-1 ( A,C ) Overall ( A ) or GADD34-specific ( C ) PP1 phosphatase activity in whole cell lysates of DCs 1 h after stimulation with poly(I:C)-LV and/or receptor crosslinking with isotype or DC-SIGN-specific antibodies (left panels) or 24 h after infection with rMV KS or rMV IC323 (right panels), in the absence or presence of Raf inhibitor GW5074. Data are presented as mean ± SD. ( B,E,F ) RIG-I phosphorylation at Ser8 or Thr170 and Mda5 phosphorylation at Ser88 in DCs left unstimulated; or 3 h after stimulation by receptor crosslinking with isotype or DC-SIGN-specific (antibodies ( B,F ); or 8 h after rMV KS infection ( E ), in the absence or presence of GADD34 inhibitor guanabenz (Gb) ( B ) or after GADD34 or I-1 silencing ( E,F ), as determined by flow cytometry. ( D ) I-1 phosphorylation at Ser or Thr residues, and association with PP1α or PP1γ after immunoprecipitation (IP) of I-1 from whole cell lysates of DCs left unstimulated or 3 h after infection with rMV KS , in the absence or presence of GW5074, determined by immunoblotting (IB). ( G,H ) IFN-β, MxA, and ISG15 mRNA expression by DCs 8 h after stimulation with poly(I:C)-LV and/or receptor crosslinking with isotype or DC-SIGN-specific antibodies ( G ) or 24 h after infection with rMV KS ( H ), after GADD34 or I-1 silencing, measured by real-time PCR, normalized to GAPDH, and set at 1 in MV- or poly(I:C)-LV-stimulated control-silenced cells. Data are presented as mean ± SD. *, P

Techniques Used: Activation Assay, Activity Assay, Infection, Flow Cytometry, Cytometry, Immunoprecipitation, Expressing, Real-time Polymerase Chain Reaction

3) Product Images from "RASAL2 down-regulation in ovarian cancer promotes epithelial-mesenchymal transition and metastasis"

Article Title: RASAL2 down-regulation in ovarian cancer promotes epithelial-mesenchymal transition and metastasis

Journal: Oncotarget

doi:

RASAL2 knockdown activates the Ras-ERK pathway (A) The effect of RASAL2 knockdown on Ras activation in SK-OV-3, OVCAR3 and A2780 cells was evaluated by a Ras Activation ELISA Assay Kit. All the data were normalized to the results of cells transfected with scramble-shRNA. The data are shown as the means ± SD (n = 3). (B) Phosphorylation of Raf-1, MEK1/2 and ERK1/2 in SK-OV-3, OVCAR3 and A2780 cells infected with shRASAL2-1, shRASAL2-2 or scramble-shRNA was analyzed by Western blot. Xenograft tumor sections (SK-OV-3) were also examined for levels of p-ERK by IHC (C) and for p-Raf-1 and p-MEK by Western blot (D).
Figure Legend Snippet: RASAL2 knockdown activates the Ras-ERK pathway (A) The effect of RASAL2 knockdown on Ras activation in SK-OV-3, OVCAR3 and A2780 cells was evaluated by a Ras Activation ELISA Assay Kit. All the data were normalized to the results of cells transfected with scramble-shRNA. The data are shown as the means ± SD (n = 3). (B) Phosphorylation of Raf-1, MEK1/2 and ERK1/2 in SK-OV-3, OVCAR3 and A2780 cells infected with shRASAL2-1, shRASAL2-2 or scramble-shRNA was analyzed by Western blot. Xenograft tumor sections (SK-OV-3) were also examined for levels of p-ERK by IHC (C) and for p-Raf-1 and p-MEK by Western blot (D).

Techniques Used: Activation Assay, Enzyme-linked Immunosorbent Assay, Transfection, shRNA, Infection, Western Blot, Immunohistochemistry

Related Articles

Centrifugation:

Article Title: TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-ERK MAPK signaling
Article Snippet: .. Cell lysis and western blots After treatment, cells were washed twice with PBS, lysed in lysis buffer [50 mM Tris-HCl pH 7.4, 1% Triton X-100, 1% sodium deoxycholate, 0.1% SDS, 150 mM NaCl, 1 mM EDTA, phosphatase inhibitor cocktail set II (EMD Biosciences, Calbiochem, San Diego, CA) and protease inhibitor cocktail (Roche, Mannheim, Germany)] and cleared by centrifugation at 14000 × g for 10 min. Total proteins (30 μg) were separated by SDS-PAGE, transferred onto nitrocellulose or PVDF membranes, blocked in 5% nonfat dry milk in TBST and probed with anti- Raf-1, anti- MEK1/2, anti-ERK1/2, anti-PARP (all from Cell Signaling Technology, Beverly MA), anti-phospho-MEK1/2, anti-phospho-ERK1/2, anti-vinculin and anti-GAPDH (all from Santa Cruz Biotechnology, Santa Monica, CA). .. Primary antibodies were detected with horseradish peroxidase-conjugated secondary antibodies and chemiluminescent HRP substrate (Millipore, Mississauga, ON, Canada).

Protease Inhibitor:

Article Title: TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-ERK MAPK signaling
Article Snippet: .. Cell lysis and western blots After treatment, cells were washed twice with PBS, lysed in lysis buffer [50 mM Tris-HCl pH 7.4, 1% Triton X-100, 1% sodium deoxycholate, 0.1% SDS, 150 mM NaCl, 1 mM EDTA, phosphatase inhibitor cocktail set II (EMD Biosciences, Calbiochem, San Diego, CA) and protease inhibitor cocktail (Roche, Mannheim, Germany)] and cleared by centrifugation at 14000 × g for 10 min. Total proteins (30 μg) were separated by SDS-PAGE, transferred onto nitrocellulose or PVDF membranes, blocked in 5% nonfat dry milk in TBST and probed with anti- Raf-1, anti- MEK1/2, anti-ERK1/2, anti-PARP (all from Cell Signaling Technology, Beverly MA), anti-phospho-MEK1/2, anti-phospho-ERK1/2, anti-vinculin and anti-GAPDH (all from Santa Cruz Biotechnology, Santa Monica, CA). .. Primary antibodies were detected with horseradish peroxidase-conjugated secondary antibodies and chemiluminescent HRP substrate (Millipore, Mississauga, ON, Canada).

Incubation:

Article Title: Glucobrassicin Metabolites Ameliorate the Development of Portal Hypertension and Cirrhosis in Bile Duct-Ligated Rats
Article Snippet: .. Blots were incubated with the primary antibodies (anti-eNOS, anti-iNOS (1:1000; Millipore Corporation, Billerica, MA, USA); anti-phosphorylated eNOS (peNOS, 1:1000; Cell Signaling Technology, Danvers, MA, USA), anti-phosphorylated iNOS (piNOS, 1:1000; Abcam plc, Cambridge, UK); anti-NFκB p65 (1:200; Santa Cruz Biotechnology, Santa Cruz, CA, USA); anti-IκBα (1:1000; Abcam plc); anti-phosphorylated IκBα (pIκBα, 1:1000; Cell Signaling Technology); anti-Akt, -phosphorylated Akt Ser473 (pAkt) (1:1000 and 1:2000, respectively, Cell Signaling Technology); anti-Erk, -phosphorylated Erk (pErk) (1:3000, Millipore Corporation); anti-HIF-1α (1:200; Abcam plc); anti-Raf-1, -phosphoylated-Ser-338 Raf-1 (-pRaf-1), -VEGFR2, -phosphorylated-VEGFR2 (1:1000; Cell Signaling Technology); anti-VEGF, MMP-9 (1:1000, 90 min at room temperature, Santa Cruz Biotechnology); anti-beta-actin (1:5000; Cell Signaling Technology). .. The specific proteins were detected by enhanced chemiluminescence (Immobilon Western Chemiluminescent HRP Substrate, Merk Millipore Co., Billerica, MA, USA) and scanned with a computer-assisted video densitometer and digitalized system (BioSpectrum® 600 Imaging System, Ultra-Violet Products Ltd., Upland, CA, USA).

other:

Article Title: RASAL2 down-regulation in ovarian cancer promotes epithelial-mesenchymal transition and metastasis
Article Snippet: Antibodies were obtained from the following companies: anti-RASAL2 antibody from Abcam; anti-β-actin antibody from Sigma; anti-E-cadherin, anti-vimentin, anti-claudin-1, anti-N-cadherin, anti-ZO-1, anti-Snail, anti-Slug, anti-Raf-1, anti-p-Raf-1, anti-MEK1/2, anti-p-MEK1/2, anti-ERK1/2 and anti-p-ERK1/2 antibodies from Cell Signaling.

Expressing:

Article Title: Measles virus suppresses RIG-I-like receptor activation in dendritic cells via DC-SIGN-mediated inhibition of PP1 phosphatases
Article Snippet: .. Raf-1 expression was determined with anti-Raf-1 (9422; Cell Signaling). ..

Lysis:

Article Title: TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-ERK MAPK signaling
Article Snippet: .. Cell lysis and western blots After treatment, cells were washed twice with PBS, lysed in lysis buffer [50 mM Tris-HCl pH 7.4, 1% Triton X-100, 1% sodium deoxycholate, 0.1% SDS, 150 mM NaCl, 1 mM EDTA, phosphatase inhibitor cocktail set II (EMD Biosciences, Calbiochem, San Diego, CA) and protease inhibitor cocktail (Roche, Mannheim, Germany)] and cleared by centrifugation at 14000 × g for 10 min. Total proteins (30 μg) were separated by SDS-PAGE, transferred onto nitrocellulose or PVDF membranes, blocked in 5% nonfat dry milk in TBST and probed with anti- Raf-1, anti- MEK1/2, anti-ERK1/2, anti-PARP (all from Cell Signaling Technology, Beverly MA), anti-phospho-MEK1/2, anti-phospho-ERK1/2, anti-vinculin and anti-GAPDH (all from Santa Cruz Biotechnology, Santa Monica, CA). .. Primary antibodies were detected with horseradish peroxidase-conjugated secondary antibodies and chemiluminescent HRP substrate (Millipore, Mississauga, ON, Canada).

Western Blot:

Article Title: TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-ERK MAPK signaling
Article Snippet: .. Cell lysis and western blots After treatment, cells were washed twice with PBS, lysed in lysis buffer [50 mM Tris-HCl pH 7.4, 1% Triton X-100, 1% sodium deoxycholate, 0.1% SDS, 150 mM NaCl, 1 mM EDTA, phosphatase inhibitor cocktail set II (EMD Biosciences, Calbiochem, San Diego, CA) and protease inhibitor cocktail (Roche, Mannheim, Germany)] and cleared by centrifugation at 14000 × g for 10 min. Total proteins (30 μg) were separated by SDS-PAGE, transferred onto nitrocellulose or PVDF membranes, blocked in 5% nonfat dry milk in TBST and probed with anti- Raf-1, anti- MEK1/2, anti-ERK1/2, anti-PARP (all from Cell Signaling Technology, Beverly MA), anti-phospho-MEK1/2, anti-phospho-ERK1/2, anti-vinculin and anti-GAPDH (all from Santa Cruz Biotechnology, Santa Monica, CA). .. Primary antibodies were detected with horseradish peroxidase-conjugated secondary antibodies and chemiluminescent HRP substrate (Millipore, Mississauga, ON, Canada).

SDS Page:

Article Title: Non‐canonical Raf‐1/p70S6K signalling in non–small‐cell lung cancer, et al. Non‐canonical Raf‐1/p70S6K signalling in non–small‐cell lung cancer
Article Snippet: .. The proteins were then separated on sodium dodecyl sulphate‐polyacrylamide (SDS‐PAGE) gels, transferred to a polyvinylidene fluoride (PVDF) membrane (Millipore) and probed with specific primary antibodies overnight, including anti–Raf‐1 (Cell Signalling Technology), anti‐p70S6K (Cell Signalling Technology) and the internal control anti–β‐actin (Cell Signalling Technology) or anti‐GAPDH (Santa Cruz Biotechnology). .. Horseradish peroxidase‐conjugated goat anti‐rabbit IgG (Cell Signalling Technology) was used as the secondary antibody.

Article Title: TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-ERK MAPK signaling
Article Snippet: .. Cell lysis and western blots After treatment, cells were washed twice with PBS, lysed in lysis buffer [50 mM Tris-HCl pH 7.4, 1% Triton X-100, 1% sodium deoxycholate, 0.1% SDS, 150 mM NaCl, 1 mM EDTA, phosphatase inhibitor cocktail set II (EMD Biosciences, Calbiochem, San Diego, CA) and protease inhibitor cocktail (Roche, Mannheim, Germany)] and cleared by centrifugation at 14000 × g for 10 min. Total proteins (30 μg) were separated by SDS-PAGE, transferred onto nitrocellulose or PVDF membranes, blocked in 5% nonfat dry milk in TBST and probed with anti- Raf-1, anti- MEK1/2, anti-ERK1/2, anti-PARP (all from Cell Signaling Technology, Beverly MA), anti-phospho-MEK1/2, anti-phospho-ERK1/2, anti-vinculin and anti-GAPDH (all from Santa Cruz Biotechnology, Santa Monica, CA). .. Primary antibodies were detected with horseradish peroxidase-conjugated secondary antibodies and chemiluminescent HRP substrate (Millipore, Mississauga, ON, Canada).

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  • 85
    Cell Signaling Technology Inc phosphorylated raf 1 antibodies
    Insulin activates <t>Raf-1</t> and ERK in transformed MIN6 cells. Panel A, ERK phosphorylation in MIN6 cells treated with low glucose (5 m m ) or high glucose (25 m m ) for 15 min with or without somatostatin (Soma, 1 μ m ; n = 3). Panel B, Insulin
    Phosphorylated Raf 1 Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phosphorylated raf 1 antibodies/product/Cell Signaling Technology Inc
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    Cell Signaling Technology Inc raf 1 antibody
    Activated K-Ras regulates NSC proliferation in a Raf- and Rb-dependent manner. (A) : <t>Raf-1</t> immunoprecipitation reveals that Rb binds to Raf-1 in K-Ras*-expressing NSCs. (B) : The small molecule inhibitor RRD-251 reduces K-Ras*-induced NSC hyperproliferation
    Raf 1 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/raf 1 antibody/product/Cell Signaling Technology Inc
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    Cell Signaling Technology Inc primary antibodies against braf
    Oncogenic <t>BRAF</t> fusion gene detected in MFS. a Schematic presentation of the proteins encoded by SLC37A3 , BRAF , and SLC37A3-BRAF fusion gene. MFS major facilitator superfamily, RBD RAS-binding domain, C1 phorbol esters/diacylglycerol-binding domain (C1 domain), Kinase protein kinase. b BRAF fusion induced <t>ERK</t> activation. Proteins extracted from cells transfected with retroviruses containing control, BRAF-V600E , and SLC37A3-BRAF were immunoblotted with antibodies against BRAF, phosphorylated ERK (p-ERK), ERK, and β-Actin. c Tumorigenicity of SLC37-BRAF fusion. Representative images of mice subcutaneously transplanted with NIH3T3 cells expressing empty vector or the SLC37A3-BRAF fusion. NIH3T3 cells transformed with BRAF V600E were used as a positive control
    Primary Antibodies Against Braf, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti pb raf
    Apoptotic cell-induced expression of TSP-1 in HUVEC is mediated by the <t>B-Raf/MEK/ERK</t> pathway. (A) Exposure of HUVEC to apoptotic eEND2 cells led to a rapid activation of <t>ERK1/2</t> (left) and B-Raf (right). Changes in phosphorylation were determined by calculation of the ratio of phosphorylated to unphosphorylated ERK1/2 or B-Raf protein, respectively ( n = 6). (B) Immunocytochemical staining of pERK1/2 and pB-Raf in HUVEC exposed to apoptotic eEND2 cells. Cells were counterstained with phalloidin-Alexa546 and analysed by confocal microscopy. Shown are representative micrographs of three independent experiments. Scale bars represent 50 μm. (C) Inhibition of ERK phosphorylation by U0126 or PD98059 circumvented apoptotic cell-induced enhanced TSP-1 expression in HUVEC as assessed by real-time qPCR measurement ( n = 4; ** P
    Anti Pb Raf, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Insulin activates Raf-1 and ERK in transformed MIN6 cells. Panel A, ERK phosphorylation in MIN6 cells treated with low glucose (5 m m ) or high glucose (25 m m ) for 15 min with or without somatostatin (Soma, 1 μ m ; n = 3). Panel B, Insulin

    Journal: Endocrinology

    Article Title: Acute Insulin Signaling in Pancreatic Beta-Cells Is Mediated by Multiple Raf-1 Dependent Pathways

    doi: 10.1210/en.2009-0678

    Figure Lengend Snippet: Insulin activates Raf-1 and ERK in transformed MIN6 cells. Panel A, ERK phosphorylation in MIN6 cells treated with low glucose (5 m m ) or high glucose (25 m m ) for 15 min with or without somatostatin (Soma, 1 μ m ; n = 3). Panel B, Insulin

    Article Snippet: Insulin receptor and phosphorylated Raf-1 antibodies were from Cell Signaling and phosphorylated insulin receptor, Raf-1, and insulin antibodies were from Stressgen (Ann Arbor, MI), BD Biosciences, and Linco Research (St. Charles, MO), respectively.

    Techniques: Transformation Assay

    Insulin promotes Raf-1 and ERK activation in mouse islets. A, Acute insulin signaling stimulation for 15 min in primary mouse islets with 0.2 and 200 n m insulin resulted in a loss of inhibitory phosphorylation of Raf-1 (pRaf-1) at serine 259. B, Mouse

    Journal: Endocrinology

    Article Title: Acute Insulin Signaling in Pancreatic Beta-Cells Is Mediated by Multiple Raf-1 Dependent Pathways

    doi: 10.1210/en.2009-0678

    Figure Lengend Snippet: Insulin promotes Raf-1 and ERK activation in mouse islets. A, Acute insulin signaling stimulation for 15 min in primary mouse islets with 0.2 and 200 n m insulin resulted in a loss of inhibitory phosphorylation of Raf-1 (pRaf-1) at serine 259. B, Mouse

    Article Snippet: Insulin receptor and phosphorylated Raf-1 antibodies were from Cell Signaling and phosphorylated insulin receptor, Raf-1, and insulin antibodies were from Stressgen (Ann Arbor, MI), BD Biosciences, and Linco Research (St. Charles, MO), respectively.

    Techniques: Activation Assay

    Insulin promotes Raf-1 translocation to the mitochondria. A, Insulin (0.2 n m ) promoted Raf-1 mitochondrial localization compared with serum free in mouse pancreatic β-cell (n = 3). Scale bars , 10 μm. B, A plot of Pearson correlation

    Journal: Endocrinology

    Article Title: Acute Insulin Signaling in Pancreatic Beta-Cells Is Mediated by Multiple Raf-1 Dependent Pathways

    doi: 10.1210/en.2009-0678

    Figure Lengend Snippet: Insulin promotes Raf-1 translocation to the mitochondria. A, Insulin (0.2 n m ) promoted Raf-1 mitochondrial localization compared with serum free in mouse pancreatic β-cell (n = 3). Scale bars , 10 μm. B, A plot of Pearson correlation

    Article Snippet: Insulin receptor and phosphorylated Raf-1 antibodies were from Cell Signaling and phosphorylated insulin receptor, Raf-1, and insulin antibodies were from Stressgen (Ann Arbor, MI), BD Biosciences, and Linco Research (St. Charles, MO), respectively.

    Techniques: Translocation Assay

    Endogenous Bcl-2 family members and Raf-1 form protein-protein interactions in pancreatic β-cell. A, Immunofluorescence imaging of endogenous Raf-1 and Bad in primary human and mouse β-cells. Pearson correlation r values between Raf-1

    Journal: Endocrinology

    Article Title: Acute Insulin Signaling in Pancreatic Beta-Cells Is Mediated by Multiple Raf-1 Dependent Pathways

    doi: 10.1210/en.2009-0678

    Figure Lengend Snippet: Endogenous Bcl-2 family members and Raf-1 form protein-protein interactions in pancreatic β-cell. A, Immunofluorescence imaging of endogenous Raf-1 and Bad in primary human and mouse β-cells. Pearson correlation r values between Raf-1

    Article Snippet: Insulin receptor and phosphorylated Raf-1 antibodies were from Cell Signaling and phosphorylated insulin receptor, Raf-1, and insulin antibodies were from Stressgen (Ann Arbor, MI), BD Biosciences, and Linco Research (St. Charles, MO), respectively.

    Techniques: Immunofluorescence, Imaging

    Activated K-Ras regulates NSC proliferation in a Raf- and Rb-dependent manner. (A) : Raf-1 immunoprecipitation reveals that Rb binds to Raf-1 in K-Ras*-expressing NSCs. (B) : The small molecule inhibitor RRD-251 reduces K-Ras*-induced NSC hyperproliferation

    Journal: Stem cells (Dayton, Ohio)

    Article Title: Activated K-Ras, But Not H-Ras or N-Ras, Regulates Brain Neural Stem Cell Proliferation in a Raf/Rb-Dependent Manner

    doi: 10.1002/stem.1990

    Figure Lengend Snippet: Activated K-Ras regulates NSC proliferation in a Raf- and Rb-dependent manner. (A) : Raf-1 immunoprecipitation reveals that Rb binds to Raf-1 in K-Ras*-expressing NSCs. (B) : The small molecule inhibitor RRD-251 reduces K-Ras*-induced NSC hyperproliferation

    Article Snippet: Raf-1 pull-down was confirmed by blotting with a different Raf-1 antibody (Cell Signaling, ).

    Techniques: Immunoprecipitation, Expressing

    Oncogenic BRAF fusion gene detected in MFS. a Schematic presentation of the proteins encoded by SLC37A3 , BRAF , and SLC37A3-BRAF fusion gene. MFS major facilitator superfamily, RBD RAS-binding domain, C1 phorbol esters/diacylglycerol-binding domain (C1 domain), Kinase protein kinase. b BRAF fusion induced ERK activation. Proteins extracted from cells transfected with retroviruses containing control, BRAF-V600E , and SLC37A3-BRAF were immunoblotted with antibodies against BRAF, phosphorylated ERK (p-ERK), ERK, and β-Actin. c Tumorigenicity of SLC37-BRAF fusion. Representative images of mice subcutaneously transplanted with NIH3T3 cells expressing empty vector or the SLC37A3-BRAF fusion. NIH3T3 cells transformed with BRAF V600E were used as a positive control

    Journal: Nature Communications

    Article Title: Integrated genetic and epigenetic analysis of myxofibrosarcoma

    doi: 10.1038/s41467-018-03891-9

    Figure Lengend Snippet: Oncogenic BRAF fusion gene detected in MFS. a Schematic presentation of the proteins encoded by SLC37A3 , BRAF , and SLC37A3-BRAF fusion gene. MFS major facilitator superfamily, RBD RAS-binding domain, C1 phorbol esters/diacylglycerol-binding domain (C1 domain), Kinase protein kinase. b BRAF fusion induced ERK activation. Proteins extracted from cells transfected with retroviruses containing control, BRAF-V600E , and SLC37A3-BRAF were immunoblotted with antibodies against BRAF, phosphorylated ERK (p-ERK), ERK, and β-Actin. c Tumorigenicity of SLC37-BRAF fusion. Representative images of mice subcutaneously transplanted with NIH3T3 cells expressing empty vector or the SLC37A3-BRAF fusion. NIH3T3 cells transformed with BRAF V600E were used as a positive control

    Article Snippet: Whole-cell lysates were subjected to immunoblot analysis using primary antibodies against BRAF (1:500; #14814, Cell Signaling Technology), p44/42 ERK (1:500; #4695, Cell Signaling Technology), and phosphorylated p44/42 ERK (Thr202/Tyr204) (1:500; #4370, Cell Signaling Technology).

    Techniques: Binding Assay, Activation Assay, Transfection, Mouse Assay, Expressing, Plasmid Preparation, Transformation Assay, Positive Control

    Apoptotic cell-induced expression of TSP-1 in HUVEC is mediated by the B-Raf/MEK/ERK pathway. (A) Exposure of HUVEC to apoptotic eEND2 cells led to a rapid activation of ERK1/2 (left) and B-Raf (right). Changes in phosphorylation were determined by calculation of the ratio of phosphorylated to unphosphorylated ERK1/2 or B-Raf protein, respectively ( n = 6). (B) Immunocytochemical staining of pERK1/2 and pB-Raf in HUVEC exposed to apoptotic eEND2 cells. Cells were counterstained with phalloidin-Alexa546 and analysed by confocal microscopy. Shown are representative micrographs of three independent experiments. Scale bars represent 50 μm. (C) Inhibition of ERK phosphorylation by U0126 or PD98059 circumvented apoptotic cell-induced enhanced TSP-1 expression in HUVEC as assessed by real-time qPCR measurement ( n = 4; ** P

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Endothelial-derived thrombospondin-1 promotes macrophage recruitment and apoptotic cell clearance

    doi: 10.1111/j.1582-4934.2009.00799.x

    Figure Lengend Snippet: Apoptotic cell-induced expression of TSP-1 in HUVEC is mediated by the B-Raf/MEK/ERK pathway. (A) Exposure of HUVEC to apoptotic eEND2 cells led to a rapid activation of ERK1/2 (left) and B-Raf (right). Changes in phosphorylation were determined by calculation of the ratio of phosphorylated to unphosphorylated ERK1/2 or B-Raf protein, respectively ( n = 6). (B) Immunocytochemical staining of pERK1/2 and pB-Raf in HUVEC exposed to apoptotic eEND2 cells. Cells were counterstained with phalloidin-Alexa546 and analysed by confocal microscopy. Shown are representative micrographs of three independent experiments. Scale bars represent 50 μm. (C) Inhibition of ERK phosphorylation by U0126 or PD98059 circumvented apoptotic cell-induced enhanced TSP-1 expression in HUVEC as assessed by real-time qPCR measurement ( n = 4; ** P

    Article Snippet: The individual primary antibodies used were anti-p-ERK1/2 and anti-pB-Raf (1:1000 dilutions, Cell Signaling, Danvers, MA, USA).

    Techniques: Expressing, Activation Assay, Staining, Confocal Microscopy, Inhibition, Real-time Polymerase Chain Reaction