61-7400

antibody from Invitrogen Antibodies

Targeting: MAPK3 ERK1, p44erk1, p44mapk, PRKM3

Provider product page for 61-7400

Western blot

ELISA

Immunocytochemistry

Immunoprecipitation

Immunohistochemistry

Other assay

Antibody data

Antibody Data
Antigen structure
References [25]
Comments [0]
Validations
Western blot [1]
Immunocytochemistry [1]
Other assay [13]

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Product number: 61-7400 - Provider product page
Provider: Invitrogen Antibodies
Product name: ERK1/ERK2 Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Reactivity: Human, Mouse, Rat, Rabbit
Host: Rabbit
Isotype: IgG
Vial size: 100 µg
Concentration: 0.25 mg/mL
Storage: -20°C

MAPK3 protein structure - 61-7400 shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Western blot analysis following immunoprecipitation of mouse brain homogenates using Zymed's ERK1+ERK2 (MAP kinase) (Product # 61-7400, 13-6200), ERK1 (Product # 13-8600), and ERK2 (Product # 71-1800) antibodies.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 ERK2 is expressed in the majority of chondrocytes in DKO CD4 mice . (A) Chondrocytes were isolated from individual WT, Erk1 -/- .Erk2 fl/fl .CD4cre - (E1), or DKO CD4 mice and cultured in vitro . DNA was isolated and analyzed by PCR for the presence of the wild-type, floxed, or excised Erk2 allele. Tail DNA is shown as controls for the wild-type and floxed alleles, while DNA from thymocytes serves as the positive control for the excised allele. (B) Cultured chondrocytes were lysed and analyzed by western blot for ERK1, ERK2, type II collagen (Col2A1), and beta-actin. (C) Planar X-ray (left) and surgical microscopy images of a representative lesion from a DKO CD4 mouse. (D) Three microdissected tumors from individual mice greater than 20 weeks of age were analyzed by PCR to determine whether the Erk2 gene was wild-type, floxed, or excised by Cre recombinase. DNA from DKO CD4 thymocytes is shown as a positive control for Erk2 excision, while tail DNA is a negative control for excision. The first row contains primers that amplify the wild-type, floxed, or excised alleles, the second row is primers that only amplify the excised allele. The third row contains primers that amplify the wild-type or floxed alleles.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 In vitro effect of EGFR inhibitor erlotinib and decreased tumours growth in vivo after combined treatment with PARP inhibitor and erlotinib A. Western blot analysis of p-ERK-1/2 expression levels at different times following erlotinib treatment.. B,C. B,C. U87MG cells were treated with erlotinib alone or combined with PJ34 during 72 hours. (B) p-ERK-1/2 expression was measured by Western Blot. (C) MTT reduction was analysed. *** p < 0.001 versus control group by t-test. D. Mice were inoculated with U87MG-luciferase human cell line. Localization and intensity of luciferase expression were monitored by in vivo bioluminiscence imaging (dpi, days post cells injection). Representation of tumours growth inhibition on the 16 th day. A statistically significant reduction is observed in the combined treatment of PJ34 and erlotinib. * p < 0.05 versus control group by t-test. Data are represented as mean +- SEM of 3 independent experiments.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 3 CAPN1 inhibition stabilizes NF1 levels, affecting RAS signaling and cell proliferation (A) NF1 wild type cells (A375, 74T) were treated with increasing concentrations of Calpain inhibitor I (muM) for 6 hours or with DMSO as control, and NF1 levels were tested by immunoblot. (B) NF1 mutant cells (108T, 76T) were treated with increasing concentrations of Calpain inhibitor I (muM) for 6 hours or with DMSO as control, and NF1 levels were tested by immunoblot. Ratios of NF1 levels to GAPDH were generated using Image lab (BioRad) and Microsoft Excel analysis. (C) 74T and A375 cells were treated with 3 muM or 5 muM of Calpain inhibitor I for 16 hours, respectively. Cell lysates were analyzed by western blot with the indicated antibodies. RAS-GTP levels were assessed by RAS pulldown assay after treatment with 50 muM of Calpain inhibitor I, respectively for 6 hours. (D) A375 and 74T cells were seeded in the 96 well plates with 10% FBS and cells were treatedwith 2.5 or 5 muM of Calpain inhibitor I, respectively. DMSO was used as a control for this experiment. The average cell number was measured by assessing DNA content using SYBR green I in two independent experiments with six replicates each. Error bars, s.e.m.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 4 Suppression of CAPN1 by shRNA stabilizes NF1 levels and affects Ras signaling and cell proliferation (A) Immunoblot of lysates generated from siRNA mediated CAPN1 knockdown and control tested by transient transfection of 100 nM for 72 hours. (B) Immunoblots of lysates generated from two shRNA mediated CAPN1 knockdown (shCAPN1-1 and shCAPN1-2) compared to the control vector. Quantification values are given under the blots generated by Image lab (BioRad) and Microsoft Excel analysis. (C) 74T and A375 cells stably expressing shRNA against CAPN1 (shCAPN1-1 or shCAPN1-2) were grown in 96 well plates with 10% or 2.5% FBS, respectively. The average cell number was measured by assessing DNA content using SYBR green I in two independent experiments with six replicates each. Error bars, s.e.m.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 5 Effect of acylated ghrelin on ERK1/ERK2 activation in the jejunum. Syrian Golden Hamsters were submitted to conventional chow (CD) or Western (WD) diets for 8 weeks. For the last 2 weeks of treatment, animals were continuously administered with acylated ghrelin (AG, 100 nmol/kg/day) or physiological saline. Before sacrifice, hamsters were fasted for 16 h before receiving an olive oil gavage (200 uL). Jejunum samples were homogenized in a lysis buffer and proteins lysates were analyzed by Western Blot with ERK1/ERK2 ( A,B ) and phosphoERK1/ERK2 ( A,C ) antibodies as indicated. The ratio of pERK1/2/ERK1/2 was also analyzed. ( D ) For accurate normalization, the same blot was probed with GAPDH. A representative blot is shown, illustrating an experiment in triplicate on the same gel and at the same time exposure. The results of every experiment are shown as mean +- SEM of n = 4-6 animals * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig 7 Effects of host FGFs and BIBF 1120 on EmMPK1 phosphorylation in metacestode vesicles. A , axenically cultivated metacestode vesicles were incubated in cMEM (control) or in medium without FCS (0 s), upon which FGF1 (aFGF) or FGF2 (bFGF) were added at a concentration of 10 nM for 30 sec (30s), 60 sec (60s) or 60 min (60min). Protein lysates were subsequently separated by 12% SDS-PAGE and Western blots were analysed using polyclonal antibodies against Erk-like MAP kinases (anti-ERK) or double phosphorylated Erk-like MAP kinases (anti-p-ERK). B , axenically cultivated metacestode vesicles were incubated with DMSO (negative control), 5 mM or 10 mM BIBF1120 (30 min each) and cell lysates were subsequently analysed as described above. Both experiments were performed in triplicate with similar results.