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map kinase p44 42  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc map kinase p44 42
    Map Kinase P44 42, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 13028 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/map+kinase+p44+42/pmc13016477-357-12-15?v=Cell+Signaling+Technology+Inc
    Average 99 stars, based on 13028 article reviews
    map kinase p44 42 - by Bioz Stars, 2026-08
    99/100 stars

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    Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and <t>anti-phospho-ERK1/2</t> (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001
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    Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and <t>anti-phospho-ERK1/2</t> (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001
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    Cell Signaling Technology Inc antibody cell signaling technology rrid ab 330744 p44 42 map kinase
    Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and <t>anti-phospho-ERK1/2</t> (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001
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    Cell Signaling Technology Inc p44 42 mapk erk1 2 3a7
    Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and <t>anti-phospho-ERK1/2</t> (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001
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    Image Search Results


    Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

    Journal: Molecular Biomedicine

    Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

    doi: 10.1186/s43556-025-00398-w

    Figure Lengend Snippet: Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

    Article Snippet: The following primary antibodies were used: anti-phospho-FGFR (Tyr653/Tyr654) (pFGFR) (#06–1433) from Millipore, anti-tubulin (#T6557) from Sigma-Aldrich, anti-FGFR1 (FGFR1) (#9740), anti-phospho-p44/42 (Thr202/Tyr204) MAP kinase (pERK1/2) (#9101), anti-p44/42 MAP kinase (ERK1/2) (#9102), anti-phospho-FRS2α (Tyr196) (pFRS2) (#3864), anti-vinculin (#13901), anti-phospho-PLCγ1 (Tyr783) (pPLCγ) (#14,008), anti-PLCγ1 (#5690), anti-Glut1 (#73,015) and anti-FGF1 (#3139) from Cell Signaling Technology.

    Techniques: Activity Assay, Activation Assay, Western Blot

    Impaired activation of signaling pathways by FGF1 variants due to reduced affinity for the FGFR1 (IIIc) receptor. a Serum-starved NIH 3T3 cells were stimulated with 10 ng/mL FGF1 variants in the presence of heparin (10 U/mL) for 15 min, and activation of downstream signaling cascades was detected by immunoblotting using the following antibodies: anti-phospho-FGFR (pFGFR), anti-phospho-PLCγ (pPLCγ), anti-phosphoFRS2 (pFRS2), anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2, anti-FGFR1, anti-PLCγ and anti-γTubulin antibodies were used to confirm equal loading. Representative results are shown. Densitometric analysis is presented as mean ± SEM, n = 3/4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001. b BLI analysis of the affinity of FGF1 variants for FGFR1-Fc (IIIc isoform). FGFR1-Fc was immobilized on a Protein A sensor and its interactions (association and dissociation) with selected FGF1 mutants were analyzed in the concentration range of 100–800 nM. Curves obtained by global fitting are marked in red. Representative results are shown (n ≥ 3). The equilibrium dissociation constant (K D ) was calculated from the saturation binding curve

    Journal: Molecular Biomedicine

    Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

    doi: 10.1186/s43556-025-00398-w

    Figure Lengend Snippet: Impaired activation of signaling pathways by FGF1 variants due to reduced affinity for the FGFR1 (IIIc) receptor. a Serum-starved NIH 3T3 cells were stimulated with 10 ng/mL FGF1 variants in the presence of heparin (10 U/mL) for 15 min, and activation of downstream signaling cascades was detected by immunoblotting using the following antibodies: anti-phospho-FGFR (pFGFR), anti-phospho-PLCγ (pPLCγ), anti-phosphoFRS2 (pFRS2), anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2, anti-FGFR1, anti-PLCγ and anti-γTubulin antibodies were used to confirm equal loading. Representative results are shown. Densitometric analysis is presented as mean ± SEM, n = 3/4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001. b BLI analysis of the affinity of FGF1 variants for FGFR1-Fc (IIIc isoform). FGFR1-Fc was immobilized on a Protein A sensor and its interactions (association and dissociation) with selected FGF1 mutants were analyzed in the concentration range of 100–800 nM. Curves obtained by global fitting are marked in red. Representative results are shown (n ≥ 3). The equilibrium dissociation constant (K D ) was calculated from the saturation binding curve

    Article Snippet: The following primary antibodies were used: anti-phospho-FGFR (Tyr653/Tyr654) (pFGFR) (#06–1433) from Millipore, anti-tubulin (#T6557) from Sigma-Aldrich, anti-FGFR1 (FGFR1) (#9740), anti-phospho-p44/42 (Thr202/Tyr204) MAP kinase (pERK1/2) (#9101), anti-p44/42 MAP kinase (ERK1/2) (#9102), anti-phospho-FRS2α (Tyr196) (pFRS2) (#3864), anti-vinculin (#13901), anti-phospho-PLCγ1 (Tyr783) (pPLCγ) (#14,008), anti-PLCγ1 (#5690), anti-Glut1 (#73,015) and anti-FGF1 (#3139) from Cell Signaling Technology.

    Techniques: Activation Assay, Protein-Protein interactions, Western Blot, Concentration Assay, Binding Assay