Affinity Purified (Prepared from rabbit serum by affinity purification via sequential chromatography on phospho- and dephospho-peptide affinity columns.)
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is >95% (by SDS-PAGE).
Testing Data (Western blot analysis of COS-7 simian fibroblast-like whole cell lysate probed with Mouse anti p53 antibody followed by HRP conjugated Goat anti Mouse IgG, visualized using chemiluminescence)
Testing Data (Published customer image:Response of p53siRNA U2-OS cells to etoposide. (A) Inhibition of p53 expression in p53siRNA U2-OS. Actin was used as loading control. (B) p53siRNA U2-OS were less sensitive to etoposide when compared with parental and Ctrl U2-OS;). Student's test from three independent experiments indicated significantly higher IC50 mean values at 72 h of treatment in p53siRNA U2-OS than in Ctrl and parental U2-OS cells; p = 0.05 (C) Etoposide treatment did not induce mature miR-34a expression in p53siRNA U2-OS, as opposed to Ctrl U2-OS. (D) p53siRNA U2-OS cells presented CpG island methylation (M-MSP) of one of the two alleles of miR-34a. In Ctrl U2-OS both alleles were unmethylated. (E) p53siRNA transfection determined lengthening of G2/M phase after 48 h of etoposide treatment when compared to untreated cells. (F) Western blot of cyclin D1 and CDK4 in p53siRNA cell showed increased amount of CDK4 linked to cyclin D1 and total CDK4 after etoposide treatment when compared to control. No differences in cyclin D1 levels were seen. Ctrl = siRNA negative control duplex; C = Untreated cells; T = Etoposide treated cells.From: Novello C, Pazzaglia L, Conti A, Quattrini I, Pollino S, et al. (2014) p53-Dependent Activation of microRNA-34a in Response to Etoposide-Induced DNA Damage in Osteosarcoma Cell Lines Not Impaired by Dominant Negative p53 Expression. PLoS ONE 9(12): e114757.)
Testing Data (Published customer image: p53 protein expression in OS cells. wt-p53 U2-OS, U2-OS transfected with empty vector (U2-OS/e) and p53-impaired U2-OS175 cells were positive to anti-p53 that binds the transactivation site of N-terminal domain (aa20-25), with increased expression in U2-OS175 cells. U2-OS and U2-OS/e also presented accumulation of p53 phosphorylated at Ser20 residue (p-p53). MG63 and Saos-2 were negative to both antibodies. Actina was used as loading control.From: Novello C, Pazzaglia L, Conti A, Quattrini I, Pollino S, et al. (2014) p53-Dependent Activation of microRNA-34a in Response to Etoposide-Induced DNA Damage in Osteosarcoma Cell Lines Not Impaired by Dominant Negative p53 Expression. PLoS ONE 9(12): e114757.)
Immunohistochemistry (IHC) (Formalin-fixed and paraffin-embedded human brain tissue reacted with FMR1 Antibody (N-term), which was peroxidase-conjugated to the secondary antibody, followed by DAB staining. This data demonstrates the use of this antibody for immunohistochemistry; clinical relevance has not been evaluated.)
Western Blot (WB) (Western blot analysis of FMR1 Antibody (N-term)MBS9207834 in mouse lung tissue lysates (35ug/lane). FMR1 (arrow) was detected using the purified Pab.)
Flow Cytometry (FC/FACS) (FMR1 Antibody (N-term) flow cytometric analysis of NCI-H460 cells (right histogram) compared to a negative control cell (left histogram).FITC-conjugated goat-anti-rabbit secondary antibodies were used for the analysis.)
Testing Data (Western blot analysis of COS-7 simian fibroblast-like whole cell lysate probed with Mouse anti p53 antibody (MBS212262) followed by HRP conjugated Goat anti Mouse IgG, visualized using chemiluminescence)
Testing Data (Published customer image:Response of p53siRNA U2-OS cells to etoposide. (A) Inhibition of p53 expression in p53siRNA U2-OS. Actin was used as loading control. (B) p53siRNA U2-OS were less sensitive to etoposide when compared with parental and Ctrl U2-OS;). Student's test from three independent experiments indicated significantly higher IC50 mean values at 72 h of treatment in p53siRNA U2-OS than in Ctrl and parental U2-OS cells; p = 0.05 (C) Etoposide treatment did not induce mature miR-34a expression in p53siRNA U2-OS, as opposed to Ctrl U2-OS. (D) p53siRNA U2-OS cells presented CpG island methylation (M-MSP) of one of the two alleles of miR-34a. In Ctrl U2-OS both alleles were unmethylated. (E) p53siRNA transfection determined lengthening of G2/M phase after 48 h of etoposide treatment when compared to untreated cells. (F) Western blot of cyclin D1 and CDK4 in p53siRNA cell showed increased amount of CDK4 linked to cyclin D1 and total CDK4 after etoposide treatment when compared to control. No differences in cyclin D1 levels were seen. Ctrl = siRNA negative control duplex; C = Untreated cells; T = Etoposide treated cells.From: Novello C, Pazzaglia L, Conti A, Quattrini I, Pollino S, et al. (2014) p53-Dependent Activation of microRNA-34a in Response to Etoposide-Induced DNA Damage in Osteosarcoma Cell Lines Not Impaired by Dominant Negative p53 Expression. PLoS ONE 9(12): e114757.)
Testing Data (Published customer image: p53 protein expression in OS cells. wt-p53 U2-OS, U2-OS transfected with empty vector (U2-OS/e) and p53-impaired U2-OS175 cells were positive to anti-p53 that binds the transactivation site of N-terminal domain (aa20-25), with increased expression in U2-OS175 cells. U2-OS and U2-OS/e also presented accumulation of p53 phosphorylated at Ser20 residue (p-p53). MG63 and Saos-2 were negative to both antibodies. Actina was used as loading control.From: Novello C, Pazzaglia L, Conti A, Quattrini I, Pollino S, et al. (2014) p53-Dependent Activation of microRNA-34a in Response to Etoposide-Induced DNA Damage in Osteosarcoma Cell Lines Not Impaired by Dominant Negative p53 Expression. PLoS ONE 9(12): e114757.)
Immunohistochemistry (IHC) (MBS9600908 at 1/100 staining human Testis tissue sections by IHC-P. The tissue was formaldehyde fixed and a heat mediated antigen retrieval step in citrate buffer was performed. The tissue was then blocked and incubated with the antibody for 1.5 hours at 22 degree C. An HRP conjugated goat anti-rabbit antibody was used as the secondary.)
Western Blot (WB) (Western blot analysis of Phospho-Myb (Ser532) Antibody expression in mouse lung and mouse spleen tissues lysates.)
Immunofluorescence (IF) (MBS9600908 staining HeLa cells by IF/ICC. The sample were fixed with PFA and permeabilized in 0.1% Triton X-100, then blocked in 10% serum for 45 minutes at 25 degree C. The primary antibody was diluted at 1/200 and incubated with the sample for 1 hour at 37 degree C. An Alexa Fluor 594 conjugated goat anti-rabbit IgG (H+L) antibody, diluted at 1/600, was used as secondary antibody.)
Western Blot (WB) (Western blot analysis of Myb expression in 293 whole cell lysates, The lane on the left is treated with the antigen-specific peptide.)
Immunofluorescene (IF) (MBS9601758 staining HeLa cells by IF/ICC. The sample were fixed with PFA and permeabilized in 0.1% Triton X-100, then blocked in 10% serum for 45 minutes at 25 degree C. The primary antibody was diluted at 1/200 and incubated with the sample for 1 hour at 37 degree C. An Alexa Fluor 594 conjugated goat anti-rabbit IgG (H+L) antibody, diluted at 1/600, was used as secondary antibody.)
Immunohistochemistry (IHC) (MBS9604409 at 1/100 staining Mouse liver tissue by IHC-P. The sample was formaldehyde fixed and a heat mediated antigen retrieval step in citrate buffer was performed. The sample was then blocked and incubated with the antibody for 1.5 hours at 22 degree C. An HRP conjugated goat anti-rabbit antibody was used as the secondary.)
Western Blot (WB) (Western blot analysis of Myb using HeLa whole cell lysates)
Immunofluorescence (IF) (MBS9604409 staining MCF7 by IF/ICC. The sample were fixed with PFA and permeabilized in 0.1% Triton X-100, then blocked in 10% serum for 45 minutes at 25 degree C. The primary antibody was diluted at 1/200 and incubated with the sample for 1 hour at 37 degree C. An Alexa Fluor 594 conjugated goat anti-rabbit IgG (H+L) Ab, diluted at 1/600, was used as the secondary antibody.)
Immunohistochemistry (IHC) (Rabbit Anti-SOCS1 AntibodyParaffin Embedded Tissue: Human KidneyCellular Data: Epithelial cells of renal tubuleAntibody Concentration: 4.0-8.0 ug/mlMagnification: 400X)
Western Blot (WB) (Host: MouseTarget Name: SOCS1Sample Tissue: Mouse PancreasAntibody Dilution: 1ug/ml)
Western Blot (WB) (Lanes:1. Mouse WT brain extract (80ug) 2. Rat brain extract (80ug)Primary Antibody Dilution:2ug/mlSecondary Antibody:IRDye 800CW goat anti-rabbit from Li-COR BioscienceSecondary Antibody Dilution:1: 20,000Gene Name:SOCS1Submitted by:Dr. Yuzhi Chen, University of Arkansas for Medical Science)
Western Blot (WB) (SOCS1 antibody - N-terminal region validated by WB using Huh7 Cells transfected with microRNA at 1:1000.)
Western Blot (WB) (SOCS1 antibody - N-terminal region validated by WB using Jurkat cell lysate at 0.2-1 ug/ml.)
Western Blot (WB) (WB Suggested Anti-SOCS1 Antibody Titration: 1.25ug/mlSample Type: Jurkat Lysate (20ug)ÂSample Type: Jurkat cell lysate)
Testing Data
Western Blot (WB) (TNRC6A antibody (MBS5300571) used at 1 ug/ml to detect target protein.)
Western Blot (WB) (DND1 Antibody (Center) western blot analysis in Hela cell line lysates (35ug/lane).This demonstrates the DND1 antibody detected the DND1 protein (arrow).)
Western Blot (WB) (RNASEN antibody (MBS5302214) used at 1 ug/ml to detect target protein.)
Western Blot (WB) (Western Blot (WB) analysis of ALPK1 polyclonal antibody at 1:500 dilutionLane1:L02 whole cell lysate (40ug) Lane2:A2780 whole cell lysate (40ug) Lane3:H1792 whole cell lysate (40ug) Lane4:AML-12 whole cell lysate (40ug))
Immunohistochemistry (IHC) (The image is immunohistochemistry of paraffin-embedded Human liver cancer tissue using 47014(DAGLA Antibody) at dilution 1/20. (Original magnification: 200))
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