AHB0052

antibody from Invitrogen Antibodies

Targeting: INS IDDM1, IDDM2

Provider product page for AHB0052

Western blot

ELISA

Immunohistochemistry

Blocking/Neutralizing

Other assay

Antibody data

Antibody Data
Antigen structure
References [78]
Comments [0]
Validations
Western blot [2]
Other assay [9]

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Product number: AHB0052 - Provider product page
Provider: Invitrogen Antibodies
Product name: Oligomer A11 Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Other
Description: This antibody recognizes amino acid sequence-independent oligomers of proteins or peptides. A11 does not recognize monomers or mature fibers of proteins or peptides. A11 reacts with soluble AB42 oligomers and does not react with soluble low molecular weight AB40 or AB40 fibrils. A11 recognizes oligomeric species of several other amyloidogenic polypeptides including AB42, human insulin, prion, polyglutamine, lysozyme, alpha-synuclein and yeast prion Sup35. Oligomeric AB42 is recommended as a positive control, monomeric and fibrillar AB42 as negative controls.
Reactivity: Human, Mouse, Rat
Host: Rabbit
Isotype: IgG
Vial size: 50 µg
Concentration: 1.0 mg/mL
Storage: Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.

INS protein structure - AHB0052 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: Figure 5 GTM-1 rescues Abeta and Tau pathology in AD mice. A-B, GTM-1 (6 mg/kg/day) or vehicle (VEH) was administered to five-month-old 3XTg-AD mice daily for 8 weeks. The average body weight (A) and total food consumed for 8 weeks (B) was recorded. C-D, F-G, 5-month-old 3XTg-AD mice (C, D) or 15-month-old 3XTg-AD mice (F, G) were treated with GTM-1 (3 mg/kg/day) daily for 8 weeks. The insoluble and soluble Abeta42 (C, D) levels were measured using a sandwich ELISA. E, Brain proteins were obtained from 8 different 3xTg-AD mice treated with GTM-1 and 8 different 3xTg-AD mice treated with vehicle after 8 weeks of treatment. The endogenous expression of APP, C99 and C83 were assessed using western blotting analyses. CT (control treatment) mice fed with a normal (vehicle) diet. Stars indicate significant differences between the model group and control or treatment groups for that time point. *P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 5 Nec-1 decreases diffuse plaques and Abeta oligomers in the brains of APP / PS 1 mice A Immunohistochemical analysis of cortical and hippocampal regions of the brains in wild-type (Wt) and APP/PS1 mice after administration of Nec-1 (6.25 mg/kg) or vehicle (2.5% DMSO in PBS). Diffuse plaques in the brain sections were stained by anti-Abeta antibody (clone 6E10, green colour) and anti-GFAP antibody (red colour). Hoechst 33342 (blue colour) was applied for nuclear counterstaining. Scale bars = 200 mum. B-D Dot blot analysis of total Abeta (anti-Abeta: clone 6E10, also recognizes APP) and protein oligomer (anti-amyloidogenic protein oligomer A11) in the cortical (B) and hippocampal (C) region of indicated groups. (D) Quantification analysis of total Abeta and protein oligomer in the cortical and hippocampal region of indicated groups. Relative intensity of each band was determined by densitometry of dot blots (B and C) using ImageJ software and normalized to vehicle-administered APP/PS1 mouse group. All data are representative results of at least three independent experiments. E Sandwich ELISA of Abeta-soluble and Abeta-insoluble fractions from cortical and hippocampal lysates of APP/PS1 mice. Three brain lysates per group were analysed. F Western blot analyses of cortical and hippocampal lysates from APP/PS1 mice for APP and sAPPalpha expression. G ThT assays for the inhibition of Abeta aggregation. Fluorescence intensity was normalized to Abeta aggregates (100%, day 5).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 1 Amyloid burden increases with age in the retina of App NL - G - F mice. a , b Amyloid ELISA on retinal lysates of App NL - G - F mice shows accumulation of soluble Abeta 42 from 3 months of age, which rises up till 24 months. Levels of insoluble Abeta 42 only start to rise at 12 months. Accumulation of soluble, but not insoluble, Abeta 40 is seen at all ages yet does not progress with age. One-way ANOVA with Dunnett's multiple comparisons test (F 5,28 = 6.686, p = 0.0006 for soluble Abeta 42 ; F 5,27 = 20.27, p < 0.0001 for insoluble Abeta 42 ); n = 5-6. c Eighteen-month-old APP/PS1 mice have comparable soluble Abeta 42 levels yet lower levels of insoluble Abeta 42 and higher soluble Abeta 40 than App NL - G - F mice of the same age. n = 5. Of note, human Abeta levels are undetectable in the retinas of WT mice and therefore these controls are not shown. d - i Abeta immunostainings with antibodies 82E1 ( d - f ) and 6E10 ( g - i ) on retinal wholemounts of 18-month-old WT ( d , g ) and App NL - G - F mice ( e , f , h , i ) reveal the presence of Abeta plaques in App NL - G - F mice only. f Example of a reconstruction of the z-plane of the image in panel e, with 82E1 and DAPI nuclear counterstaining, showing that Abeta plaques mainly localize to the inner plexiform layer. j Representative example of a retinal wholemount on which 6E10-positive Abeta plaques are depicted with dots to illustrate plaque distribution in the retina. k Abeta plaques in the cerebral cortex of an

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 4 alphaS fibrils gradually release oligomers that are ultimately responsible for their toxicity. a Dot-blot analysis of alphaS species probed with conformational specific antibody A11 (AHB0052, Thermo Fisher Scientific), OC (AB2286, Sigma-Aldrich), conformation-insensitive polyclonal anti-alphaS antibody (ab52168, Abcam) and conformation-insensitive monoclonal 211 antibody specific for human alphaS (sc12767, Santa Cruz Biotechnology). b Representative confocal microscope images showing SF (at 0.3 muM) incubated in CM without cells in wells containing a glass coverslip for 0-24 h at 37 degC. Representative images of OB* incubated for 24 h were also shown as positive control. The green-fluorescent signals derive from the staining with mouse monoclonal 211 anti-alphaS antibodies and rabbit anti-oligomer A11 polyclonal antibodies, in the first and second rows, respectively, and then Alexa-Fluor 514-conjugated anti-mouse or anti-rabbit secondary antibodies (three independent experiments with one internal replicate). c Representative confocal scanning microscope images showing human iPSC-derived dopaminergic neurons treated for 24 h with OB*/SF/LF at 0.3 uM. Red and green fluorescence indicates mouse anti-MAP-2 antibodies (ab11267, Abcam) and the A11-positive prefibrillar oligomers, respectively. d Representative confocal scanning microscope images showing the median sections of SH-SY5Y cells treated for the lengths of time indicated with OB*/SF/LF at 0.3 uM. Red and green flu

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: FIGURE 8 Reduced 26S proteasome activity was detected in U-box - /- fish. (A) Chymotrypsin-like activity was measured in brain tissues of U-box - /- and wild-type fish at 6 and 24 months ( n = 4). Statistically significant differences are shown by asterisks ( * p < 0.05; ** p < 0.01; *** p < 0.001, Student's t -test). (B) Oligomer expression quantified from dot blot analysis in brain tissues of U-box - /- and wild-type fish at 6 and 24 months ( n = 3). Data shown are means and error bars indicate standard deviations.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1. LRRK2 R1441G KI mutation caused an age-dependent increase of SNCA oligomers in mouse brain striatum and cortex. (a) (i) Layout of example dot blots shown below, (ii) example of amyloid-like oligomer ('A11') dot blots, (iii) example of total SNCA dot blots, (iv) relative levels of total SNCA, (v) relative levels of amyloid-like oligomers in soluble striatal lysates extracted from LRRK2 R1441G KI mice and their WT littermates at 3, 12, 15 and 18 months (N = 7). Each data point represents measurement of 1mug striatal lysate from each individual mouse. (vi) Predicted rate of increase of 'A11' oligomer levels with age in LRRK2 KI mice was significantly higher than that in WT mice as estimated by mathematical fitting of their corresponding growth curves. Predicted doubling time of oligomer formation in KI mice was 15.3 months (95% CI = 10.4 to 29.13), as compared with 32.6 months (95% CI = 18.39 to 143.9) for WT mice. (b) (i) SNCA oligomer ELISA standard curve. Levels of SNCA oligomer in (ii) striatal soluble lysates, and (iii) cortical soluble lysates from LRRK2 R1441G KI mice and their age-matched WT controls determined by a sandwich-ELISA. Quantification of SNCA oligomer in samples was based on (i) a standard curve generated from purified recombinant SNCA oligomer standards (Figure S1). Data are expressed as mean +- S.E.M. Statistical significance at the level of *p < 0.05 and **p < 0.01, as compared to WT controls by post-hoc multiple comparison following two-way ANOV

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 10 Relative hippocampal levels of amyloid beta (Abeta) and amyloid precursor protein (APP) in control and Cr-supplemented 3xTg mice. Representative Western blots detecting Abeta (and APP in some cases) with the antibodies ( A ) 4G8, ( C ) moc64, ( E ) A11, and ( G ) moc87. Total protein (TP) was measured with Ponceau S staining (representative bands shown to indicate sample loading). Bar graphs ( B , D , F , H ) depict densitometry values after normalization to total protein bands and expressed as the percentage change from female control-fed means (100%) +- SD. ANOVA or Kruskal-Wallis; n = 3-4. * p < 0.05; ** p < 0.01.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 13 Correlational analyses between Cr and Alzheimer's disease- (AD) related protein levels. Pearson correlation coefficients between hippocampal Cr levels and relative normalized densitometry values from Western blot experiments measuring amyloid beta (Abeta) species and/or APP with antibodies ( A - C ) 4G8, ( D - H ) moc64, ( I ) A11, and ( J - M ) moc87 or ( N , O ) AT8 to measure hyperphosphorylated tau in control-fed male (black squares) and female (gray squares) 3xTg mice, as well as female 3xTg mice on a Cr-supplemented (white squares) diet. Note: n = 3-4, * p < 0.05, # p < 0.01.