anti-mek cst: Search Results


anti p mek1 2  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc anti p mek1 2
Anti P Mek1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/Phospho-MEK1%2F2+(Ser217%2F221)+Antibody/pm25780035-63-14-16
Average 96 stars, based on 1 article reviews
anti p mek1 2 - by Bioz Stars, 2026-09
96/100 stars
  Buy from Supplier
anti mek1 2  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc anti mek1 2
Anti Mek1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/MEK1%2F2+Mouse+mAb/pmc11366001-260-64-65
Average 96 stars, based on 1 article reviews
anti mek1 2 - by Bioz Stars, 2026-09
96/100 stars
  Buy from Supplier
p mek  (Cell Signaling Technology Inc)
99
Cell Signaling Technology Inc p mek
P Mek, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/Anti-rabbit+IgG/10__1158_slash_0008___5472__can___16___3126-101-27-31
Average 99 stars, based on 1 article reviews
p mek - by Bioz Stars, 2026-09
99/100 stars
  Buy from Supplier
anti mek 1 2  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc anti mek 1 2
Anti Mek 1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/MEK1%2F2+Rabbit+mAb/pmc05528655-173-64-68
Average 95 stars, based on 1 article reviews
anti mek 1 2 - by Bioz Stars, 2026-09
95/100 stars
  Buy from Supplier
anti pmek  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc anti pmek
Anti Pmek, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/Phospho-MEK1%2F2+(Ser217%2F221)+Rabbit+mAb/10__1158_slash_0008___5472__can___20___0448-94-26-27
Average 96 stars, based on 1 article reviews
anti pmek - by Bioz Stars, 2026-09
96/100 stars
  Buy from Supplier
anti phospho mek1 2  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc anti phospho mek1 2
Anti Phospho Mek1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/MEK1%2F2+Antibody/pmc11218313-122-38-41
Average 96 stars, based on 1 article reviews
anti phospho mek1 2 - by Bioz Stars, 2026-09
96/100 stars
  Buy from Supplier
mek  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc mek
Acute 6-OH–BDE-47 exposure impairs <t>MEK–ERK</t> signaling. A, top panel: synaptosomes were prepared from neurons acutely exposed (20 min pre-treatment) to 5 μm 6-OH with and without Bic + 4AP stimulus (10 min). Levels of the CaMK1 target pSynapsin1(serine 9) were assessed via Western blotting. n = 2. Bottom panel: to reproduce a previously reported effect linking CaMK1 to MEK–ERK activity (70), neurons were acutely exposed (60 min pre-treatment) to the CaMKK inhibitor STO-609 prior to treatment with Bic + 4AP for 10 min (indicated as +B10′). Inhibition of pERK induction was assessed by Western blotting and is quantified below. n = 3, p value generated by unpaired one-tailed t test. B, cells acutely exposed (20 min pre-treatment) to BDE-47 or one of its hydroxylated metabolites were stimulated with Bic + 4AP for 10 min before collecting whole-cell lysates. Activation of MEK–ERK signaling was assessed by Western blotting, measuring pERK <t>and</t> <t>pMEK</t> levels. Note, the lower band in the MEK panel is the ERK band visualized on the same blot. Quantification relative to total ERK and MEK is shown below representative blots. n = 3–6, p values generated by one-way ANOVA with post hoc LSD. pERK quantification: treatment F(7,22) = 9.822, p < 0.0001. pMEK quantification: treatment F(7,16) = 7.805, p = 0.0004. C, same experimental design as in B., but neurons were stimulated with TTX + PMA to induce MEK–ERK signaling synapse-independently. n = 3. pERK quantification: treatment F(7,16) = 37.95, p < 0.0001.
Mek, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/MEK1+Mouse+mAb/pmc07196656-460-43-44
Average 95 stars, based on 1 article reviews
mek - by Bioz Stars, 2026-09
95/100 stars
  Buy from Supplier
antimek  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc antimek
Acute 6-OH–BDE-47 exposure impairs <t>MEK–ERK</t> signaling. A, top panel: synaptosomes were prepared from neurons acutely exposed (20 min pre-treatment) to 5 μm 6-OH with and without Bic + 4AP stimulus (10 min). Levels of the CaMK1 target pSynapsin1(serine 9) were assessed via Western blotting. n = 2. Bottom panel: to reproduce a previously reported effect linking CaMK1 to MEK–ERK activity (70), neurons were acutely exposed (60 min pre-treatment) to the CaMKK inhibitor STO-609 prior to treatment with Bic + 4AP for 10 min (indicated as +B10′). Inhibition of pERK induction was assessed by Western blotting and is quantified below. n = 3, p value generated by unpaired one-tailed t test. B, cells acutely exposed (20 min pre-treatment) to BDE-47 or one of its hydroxylated metabolites were stimulated with Bic + 4AP for 10 min before collecting whole-cell lysates. Activation of MEK–ERK signaling was assessed by Western blotting, measuring pERK <t>and</t> <t>pMEK</t> levels. Note, the lower band in the MEK panel is the ERK band visualized on the same blot. Quantification relative to total ERK and MEK is shown below representative blots. n = 3–6, p values generated by one-way ANOVA with post hoc LSD. pERK quantification: treatment F(7,22) = 9.822, p < 0.0001. pMEK quantification: treatment F(7,16) = 7.805, p = 0.0004. C, same experimental design as in B., but neurons were stimulated with TTX + PMA to induce MEK–ERK signaling synapse-independently. n = 3. pERK quantification: treatment F(7,16) = 37.95, p < 0.0001.
Antimek, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/MEK1%2F2+Rabbit+mAb/10__1096_slash_fj__202101044rrr-20-99-102
Average 96 stars, based on 1 article reviews
antimek - by Bioz Stars, 2026-09
96/100 stars
  Buy from Supplier
rabbit anti p mek1  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc rabbit anti p mek1
Acute 6-OH–BDE-47 exposure impairs <t>MEK–ERK</t> signaling. A, top panel: synaptosomes were prepared from neurons acutely exposed (20 min pre-treatment) to 5 μm 6-OH with and without Bic + 4AP stimulus (10 min). Levels of the CaMK1 target pSynapsin1(serine 9) were assessed via Western blotting. n = 2. Bottom panel: to reproduce a previously reported effect linking CaMK1 to MEK–ERK activity (70), neurons were acutely exposed (60 min pre-treatment) to the CaMKK inhibitor STO-609 prior to treatment with Bic + 4AP for 10 min (indicated as +B10′). Inhibition of pERK induction was assessed by Western blotting and is quantified below. n = 3, p value generated by unpaired one-tailed t test. B, cells acutely exposed (20 min pre-treatment) to BDE-47 or one of its hydroxylated metabolites were stimulated with Bic + 4AP for 10 min before collecting whole-cell lysates. Activation of MEK–ERK signaling was assessed by Western blotting, measuring pERK <t>and</t> <t>pMEK</t> levels. Note, the lower band in the MEK panel is the ERK band visualized on the same blot. Quantification relative to total ERK and MEK is shown below representative blots. n = 3–6, p values generated by one-way ANOVA with post hoc LSD. pERK quantification: treatment F(7,22) = 9.822, p < 0.0001. pMEK quantification: treatment F(7,16) = 7.805, p = 0.0004. C, same experimental design as in B., but neurons were stimulated with TTX + PMA to induce MEK–ERK signaling synapse-independently. n = 3. pERK quantification: treatment F(7,16) = 37.95, p < 0.0001.
Rabbit Anti P Mek1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/Phospho-MEK1+(Thr292)+Rabbit+mAb/pmc07998021-72-26-30
Average 93 stars, based on 1 article reviews
rabbit anti p mek1 - by Bioz Stars, 2026-09
93/100 stars
  Buy from Supplier
anti phospho mek1 2 ser217 221  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc anti phospho mek1 2 ser217 221
Acute 6-OH–BDE-47 exposure impairs <t>MEK–ERK</t> signaling. A, top panel: synaptosomes were prepared from neurons acutely exposed (20 min pre-treatment) to 5 μm 6-OH with and without Bic + 4AP stimulus (10 min). Levels of the CaMK1 target pSynapsin1(serine 9) were assessed via Western blotting. n = 2. Bottom panel: to reproduce a previously reported effect linking CaMK1 to MEK–ERK activity (70), neurons were acutely exposed (60 min pre-treatment) to the CaMKK inhibitor STO-609 prior to treatment with Bic + 4AP for 10 min (indicated as +B10′). Inhibition of pERK induction was assessed by Western blotting and is quantified below. n = 3, p value generated by unpaired one-tailed t test. B, cells acutely exposed (20 min pre-treatment) to BDE-47 or one of its hydroxylated metabolites were stimulated with Bic + 4AP for 10 min before collecting whole-cell lysates. Activation of MEK–ERK signaling was assessed by Western blotting, measuring pERK <t>and</t> <t>pMEK</t> levels. Note, the lower band in the MEK panel is the ERK band visualized on the same blot. Quantification relative to total ERK and MEK is shown below representative blots. n = 3–6, p values generated by one-way ANOVA with post hoc LSD. pERK quantification: treatment F(7,22) = 9.822, p < 0.0001. pMEK quantification: treatment F(7,16) = 7.805, p = 0.0004. C, same experimental design as in B., but neurons were stimulated with TTX + PMA to induce MEK–ERK signaling synapse-independently. n = 3. pERK quantification: treatment F(7,16) = 37.95, p < 0.0001.
Anti Phospho Mek1 2 Ser217 221, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/Phospho-MEK1%2F2+(Ser217%2F221)+Rabbit+mAb/pmc08100665-50-25-27
Average 93 stars, based on 1 article reviews
anti phospho mek1 2 ser217 221 - by Bioz Stars, 2026-09
93/100 stars
  Buy from Supplier
anti p mek1  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc anti p mek1
Acute 6-OH–BDE-47 exposure impairs <t>MEK–ERK</t> signaling. A, top panel: synaptosomes were prepared from neurons acutely exposed (20 min pre-treatment) to 5 μm 6-OH with and without Bic + 4AP stimulus (10 min). Levels of the CaMK1 target pSynapsin1(serine 9) were assessed via Western blotting. n = 2. Bottom panel: to reproduce a previously reported effect linking CaMK1 to MEK–ERK activity (70), neurons were acutely exposed (60 min pre-treatment) to the CaMKK inhibitor STO-609 prior to treatment with Bic + 4AP for 10 min (indicated as +B10′). Inhibition of pERK induction was assessed by Western blotting and is quantified below. n = 3, p value generated by unpaired one-tailed t test. B, cells acutely exposed (20 min pre-treatment) to BDE-47 or one of its hydroxylated metabolites were stimulated with Bic + 4AP for 10 min before collecting whole-cell lysates. Activation of MEK–ERK signaling was assessed by Western blotting, measuring pERK <t>and</t> <t>pMEK</t> levels. Note, the lower band in the MEK panel is the ERK band visualized on the same blot. Quantification relative to total ERK and MEK is shown below representative blots. n = 3–6, p values generated by one-way ANOVA with post hoc LSD. pERK quantification: treatment F(7,22) = 9.822, p < 0.0001. pMEK quantification: treatment F(7,16) = 7.805, p = 0.0004. C, same experimental design as in B., but neurons were stimulated with TTX + PMA to induce MEK–ERK signaling synapse-independently. n = 3. pERK quantification: treatment F(7,16) = 37.95, p < 0.0001.
Anti P Mek1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/Phospho-MEK1+(Thr286)+Antibody/pmc07906155-181-24-26
Average 93 stars, based on 1 article reviews
anti p mek1 - by Bioz Stars, 2026-09
93/100 stars
  Buy from Supplier
rabbit anti mek1  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc rabbit anti mek1
Acute 6-OH–BDE-47 exposure impairs <t>MEK–ERK</t> signaling. A, top panel: synaptosomes were prepared from neurons acutely exposed (20 min pre-treatment) to 5 μm 6-OH with and without Bic + 4AP stimulus (10 min). Levels of the CaMK1 target pSynapsin1(serine 9) were assessed via Western blotting. n = 2. Bottom panel: to reproduce a previously reported effect linking CaMK1 to MEK–ERK activity (70), neurons were acutely exposed (60 min pre-treatment) to the CaMKK inhibitor STO-609 prior to treatment with Bic + 4AP for 10 min (indicated as +B10′). Inhibition of pERK induction was assessed by Western blotting and is quantified below. n = 3, p value generated by unpaired one-tailed t test. B, cells acutely exposed (20 min pre-treatment) to BDE-47 or one of its hydroxylated metabolites were stimulated with Bic + 4AP for 10 min before collecting whole-cell lysates. Activation of MEK–ERK signaling was assessed by Western blotting, measuring pERK <t>and</t> <t>pMEK</t> levels. Note, the lower band in the MEK panel is the ERK band visualized on the same blot. Quantification relative to total ERK and MEK is shown below representative blots. n = 3–6, p values generated by one-way ANOVA with post hoc LSD. pERK quantification: treatment F(7,22) = 9.822, p < 0.0001. pMEK quantification: treatment F(7,16) = 7.805, p = 0.0004. C, same experimental design as in B., but neurons were stimulated with TTX + PMA to induce MEK–ERK signaling synapse-independently. n = 3. pERK quantification: treatment F(7,16) = 37.95, p < 0.0001.
Rabbit Anti Mek1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti-mek+cst%3A/MEK1+Rabbit+mAb/pmc07998021-72-31-35
Average 94 stars, based on 1 article reviews
rabbit anti mek1 - by Bioz Stars, 2026-09
94/100 stars
  Buy from Supplier

Image Search Results


Acute 6-OH–BDE-47 exposure impairs MEK–ERK signaling. A, top panel: synaptosomes were prepared from neurons acutely exposed (20 min pre-treatment) to 5 μm 6-OH with and without Bic + 4AP stimulus (10 min). Levels of the CaMK1 target pSynapsin1(serine 9) were assessed via Western blotting. n = 2. Bottom panel: to reproduce a previously reported effect linking CaMK1 to MEK–ERK activity (70), neurons were acutely exposed (60 min pre-treatment) to the CaMKK inhibitor STO-609 prior to treatment with Bic + 4AP for 10 min (indicated as +B10′). Inhibition of pERK induction was assessed by Western blotting and is quantified below. n = 3, p value generated by unpaired one-tailed t test. B, cells acutely exposed (20 min pre-treatment) to BDE-47 or one of its hydroxylated metabolites were stimulated with Bic + 4AP for 10 min before collecting whole-cell lysates. Activation of MEK–ERK signaling was assessed by Western blotting, measuring pERK and pMEK levels. Note, the lower band in the MEK panel is the ERK band visualized on the same blot. Quantification relative to total ERK and MEK is shown below representative blots. n = 3–6, p values generated by one-way ANOVA with post hoc LSD. pERK quantification: treatment F(7,22) = 9.822, p < 0.0001. pMEK quantification: treatment F(7,16) = 7.805, p = 0.0004. C, same experimental design as in B., but neurons were stimulated with TTX + PMA to induce MEK–ERK signaling synapse-independently. n = 3. pERK quantification: treatment F(7,16) = 37.95, p < 0.0001.

Journal: The Journal of Biological Chemistry

Article Title: Certain ortho-hydroxylated brominated ethers are promiscuous kinase inhibitors that impair neuronal signaling and neurodevelopmental processes

doi: 10.1074/jbc.RA119.011138

Figure Lengend Snippet: Acute 6-OH–BDE-47 exposure impairs MEK–ERK signaling. A, top panel: synaptosomes were prepared from neurons acutely exposed (20 min pre-treatment) to 5 μm 6-OH with and without Bic + 4AP stimulus (10 min). Levels of the CaMK1 target pSynapsin1(serine 9) were assessed via Western blotting. n = 2. Bottom panel: to reproduce a previously reported effect linking CaMK1 to MEK–ERK activity (70), neurons were acutely exposed (60 min pre-treatment) to the CaMKK inhibitor STO-609 prior to treatment with Bic + 4AP for 10 min (indicated as +B10′). Inhibition of pERK induction was assessed by Western blotting and is quantified below. n = 3, p value generated by unpaired one-tailed t test. B, cells acutely exposed (20 min pre-treatment) to BDE-47 or one of its hydroxylated metabolites were stimulated with Bic + 4AP for 10 min before collecting whole-cell lysates. Activation of MEK–ERK signaling was assessed by Western blotting, measuring pERK and pMEK levels. Note, the lower band in the MEK panel is the ERK band visualized on the same blot. Quantification relative to total ERK and MEK is shown below representative blots. n = 3–6, p values generated by one-way ANOVA with post hoc LSD. pERK quantification: treatment F(7,22) = 9.822, p < 0.0001. pMEK quantification: treatment F(7,16) = 7.805, p = 0.0004. C, same experimental design as in B., but neurons were stimulated with TTX + PMA to induce MEK–ERK signaling synapse-independently. n = 3. pERK quantification: treatment F(7,16) = 37.95, p < 0.0001.

Article Snippet: Primary antibodies included the following antibodies: β-actin (Thermo Fisher Scientific, catalog no. AM4302, RRID:AB_2536382 ); H4 (CST catalog no. 2935, RRID:AB_1147658 ); pERK (CST catalog no. 4370, RRID:AB_2315112 ); ERK (CST catalog no. 4696, RRID:AB_390780 ); pMEK (CST catalog no. 9154, RRID:AB_2138017 ); MEK (CST catalog no. 2352, RRID:AB_10693788 ); synapsin1 (SySy catalog no. 106011, RRID:AB_2619772 );PSD-95 (NeuroMab catalog no. 75-028, RRID:AB_2292909 ); gephyrin (SySy catalog no. 147111, RRID:AB_887719 ); synaptotagmin6 (NeuroMab catalog no. 75-271, RRID:AB_11001830 ); and synaptophysin1(SySy catalog no. 101011, RRID:AB_887824 ).

Techniques: Western Blot, Activity Assay, Inhibition, Generated, One-tailed Test, Activation Assay