phosphorylated proteins braf (p-braf, cat Search Results


p braf s445  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc p braf s445
A Time-course analysis of p-Raf-1 S338 , p-Raf-1 S259 , p-MEK1 T292 , p-ERK1/2 T202/Y204 , <t>BRAF</t> <t>and</t> <t>p-BRAF</t> <t>S445</t> in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. B Dynamics of Raf-1 activation and BRAF inactivation in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. p-Raf-1 S338 band density was normalized to actin and then normalized to t = 6 h. p-BRAF S445 band density was normalized to actin and then normalized to t = 0. C Endogenous interaction between Raf-1 and BRAF in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 3 h or 6 h was examined by co-immunoprecipitation assay. D Western blot analysis of ERK1/2, p-ERK1/2 T202/Y204 , MEK1, p-MEK1 T292 , AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 3 h in the presence of L-779450 (20 μM). E HepG2 cells with or without PID1 overexpression upon Raf-1 knockdown were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. F Cell apoptosis in HepG2 with or without PID1 overexpression combined with Raf-1 knockdown upon Sorafenib (10 μM) treatment for 24 h was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; ns not significant.
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invitro phosphorylation gst fusion proteins  (Danaher Inc)
96
Danaher Inc invitro phosphorylation gst fusion proteins
A Time-course analysis of p-Raf-1 S338 , p-Raf-1 S259 , p-MEK1 T292 , p-ERK1/2 T202/Y204 , <t>BRAF</t> <t>and</t> <t>p-BRAF</t> <t>S445</t> in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. B Dynamics of Raf-1 activation and BRAF inactivation in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. p-Raf-1 S338 band density was normalized to actin and then normalized to t = 6 h. p-BRAF S445 band density was normalized to actin and then normalized to t = 0. C Endogenous interaction between Raf-1 and BRAF in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 3 h or 6 h was examined by co-immunoprecipitation assay. D Western blot analysis of ERK1/2, p-ERK1/2 T202/Y204 , MEK1, p-MEK1 T292 , AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 3 h in the presence of L-779450 (20 μM). E HepG2 cells with or without PID1 overexpression upon Raf-1 knockdown were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. F Cell apoptosis in HepG2 with or without PID1 overexpression combined with Raf-1 knockdown upon Sorafenib (10 μM) treatment for 24 h was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; ns not significant.
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netphos-3.1  (HealthTech Connex Inc)
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gst fusion proteins  (Covalab Inc)
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rack1a proteins  (Sabila Biosciences LLC)
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phosphorylated zebrafish rb protein  (Cell Signaling Technology Inc)
94
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antibodies against oxidative phosphorylation proteins (oxphos) ms601  (MitoSciences)
90
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gst-fusion proteins  (Promega)
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antibodies enos (against nonphosphorylated phosphorylated [ser1177] enos proteins  (Becton Dickinson)
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sod1 proteins  (Tsang MD Inc)
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phosphorylated proteins anti phospho stathmin ser38  (Cell Signaling Technology Inc)
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phosphorylated smad2 3 proteins  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc phosphorylated smad2 3 proteins
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Image Search Results


A Time-course analysis of p-Raf-1 S338 , p-Raf-1 S259 , p-MEK1 T292 , p-ERK1/2 T202/Y204 , BRAF and p-BRAF S445 in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. B Dynamics of Raf-1 activation and BRAF inactivation in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. p-Raf-1 S338 band density was normalized to actin and then normalized to t = 6 h. p-BRAF S445 band density was normalized to actin and then normalized to t = 0. C Endogenous interaction between Raf-1 and BRAF in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 3 h or 6 h was examined by co-immunoprecipitation assay. D Western blot analysis of ERK1/2, p-ERK1/2 T202/Y204 , MEK1, p-MEK1 T292 , AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 3 h in the presence of L-779450 (20 μM). E HepG2 cells with or without PID1 overexpression upon Raf-1 knockdown were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. F Cell apoptosis in HepG2 with or without PID1 overexpression combined with Raf-1 knockdown upon Sorafenib (10 μM) treatment for 24 h was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; ns not significant.

Journal: Cell Death Discovery

Article Title: Dual role of PID1 in regulating apoptosis induced by distinct anticancer-agents through AKT/Raf-1-dependent pathway in hepatocellular carcinoma

doi: 10.1038/s41420-023-01405-1

Figure Lengend Snippet: A Time-course analysis of p-Raf-1 S338 , p-Raf-1 S259 , p-MEK1 T292 , p-ERK1/2 T202/Y204 , BRAF and p-BRAF S445 in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. B Dynamics of Raf-1 activation and BRAF inactivation in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. p-Raf-1 S338 band density was normalized to actin and then normalized to t = 6 h. p-BRAF S445 band density was normalized to actin and then normalized to t = 0. C Endogenous interaction between Raf-1 and BRAF in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 3 h or 6 h was examined by co-immunoprecipitation assay. D Western blot analysis of ERK1/2, p-ERK1/2 T202/Y204 , MEK1, p-MEK1 T292 , AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 3 h in the presence of L-779450 (20 μM). E HepG2 cells with or without PID1 overexpression upon Raf-1 knockdown were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. F Cell apoptosis in HepG2 with or without PID1 overexpression combined with Raf-1 knockdown upon Sorafenib (10 μM) treatment for 24 h was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; ns not significant.

Article Snippet: Antibodies used to determine the protein expression were the following: PID1 (#27951; Signalway Antibody, Greenbelt, Maryland, USA), β-actin (#66009-1-lg; Proteintech, USA), Bcl-xL (#2764; Cell Signaling Technology, USA), Bcl2 (#12789-1-AP; Proteintech), BAD (#sc-8044 Santa Cruz Technology, Texas, USA), p-BAD S112 (#5284; Cell Signaling Technology), p-BAD S136 (#4366; Cell Signaling Technology), cytochrome c (#sc-13156; Santa Cruz Technology), cleaved caspase-3 (#9664; Cell Signaling Technology), Tom20 (#42406; Cell Signaling Technology), Raf-1 (#9422; Cell Signaling Technology), p-Raf-1 S259 (#9421; Cell Signaling Technology), p-Raf-1 S338 (#9427; Cell Signaling Technology), AKT (#4691; Cell Signaling Technology), p-AKT T308 (#13038; Cell Signaling Technology), HA-tag (#sc-7392; Santa Cruz Technology), His-tag (#sc-8036; Santa Cruz Technology), HA-tag (#14793; Cell Signaling Technology), His-tag (#12698; Cell Signal Technology), FLAG-tag (#3724; Cell Signaling Technology), FLAG-tag (#8146; Cell Signaling Technology), ERK1/2 (#4695; Cell Signaling Technology), p-ERK1/2 T202/Y204 (#4370; Cell Signaling Technology), MEK1 (#9122; Cell Signaling Technology), p-MEK1 T292 (#07-852; Upstate, Darmstadt, Germany), BRAF (#sc-5284; Santa Cruz Technology), p-BRAF S445 (#2696; Cell Signaling Technology).

Techniques: Over Expression, Activation Assay, Co-Immunoprecipitation Assay, Western Blot, Cytometry

The available tools for specific PTM and site prediction.

Journal: Environmental Microbiology

Article Title: Post‐translational modifications drive secondary metabolite biosynthesis in Aspergillus : a review

doi: 10.1111/1462-2920.16034

Figure Lengend Snippet: The available tools for specific PTM and site prediction.

Article Snippet: , NetPhos‐3.1 , https://services.healthtech.dtu.dk/service.php?NetPhos‐3.1 , Prediction of Generic phosphorylation sites in eukaryotic proteins.

Techniques: Methylation, Phospho-proteomics, Ubiquitin Proteomics