Kho0631

Manufactured by Thermo Fisher Scientific

Sourced in United States

The KHO0631 is a laboratory instrument designed for general analytical applications. It provides fundamental capabilities for sample analysis and measurement. The core function of this product is to facilitate standard laboratory operations and data collection, without making claims about its intended use or performance.

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Lab products found in correlation

9 protocols using kho0631

Quantifying Pathological Proteins in PD

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The levels of pathological proteins, including Aβ_1–42, T-tau, P-tau181t, P-tau396s and tau phosphorylated at the following positions: threonine 231 (P-tau231t) and serine 199 (P-tau199s), in CSF from PD patients and control participants were determined by using an enzyme-linked immunosorbent assay.
CSB-E10684h and CSBE12011h kits for measuring Aβ_1–42 and T-tau, respectively, were obtained from CUSABIO (Wuhan, China). KHB7031, KHB7041, KHB8051 and KHO0631 kits for measuring P-tau396s, P-tau199s, P-tau231t and P-tau181t, respectively, were obtained from Invitrogen (Carlsbad, CA, USA).

Zuo L.J., Piao Y.S., Li L.X., Yu S.Y., Guo P., Hu Y., Lian T.H., Wang R.D., Yu Q.J., Jin Z., Wang Y.J., Wang X.M., Chan P., Chen S.D., Wang Y.J, & Zhang W. (2017). Phenotype of postural instability/gait difficulty in Parkinson disease: relevance to cognitive impairment and mechanism relating pathological proteins and neurotransmitters. Scientific Reports, 7, 44872.

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Quantifying Total and Phospho-Tau in Cell Lysates

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Total tau and phosphorylated (p) tau (Threonine 181, T181) were analyzed by ELISA assay (KHB0041 and KHO0631, respectively; Invitrogen; Italy) on cell lysates. Briefly, cell lysates were obtained using a specific lysis buffer prepared adding to RIPA Buffer 1X protease inhibitor cocktail (Roche; Italy), 1% Triton X-100 (Sigma), 1% sodium orthovanadate (Sigma; UK), and 1% PMSF (Sigma). Cell lysates were quantified by the Bradford assay (Biorad; Italy), and then, 20 μg of the total lysate was diluted in 50 or 100 μl of the specific ELISA diluent and seeded into pre-coated wells. The presence of both total tau and ptau (T181) in the samples was revealed by colorimetric reaction and read at 450 nm, and concentration determined through interpolation to standard curve and reported as picograms per milliliter.

Bortolotti D., Gentili V., Rotola A., Caselli E, & Rizzo R. (2019). HHV-6A infection induces amyloid-beta expression and activation of microglial cells. Alzheimer's Research & Therapy, 11, 104.

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Quantifying Alzheimer's Protein Secretion

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To analyze protein secretion under the serum-deprived condition, the culture medium was changed to Opti-MEM and samples were incubated at 37 °C under 5% CO₂ for 12 h. The culture medium was collected and centrifuged at 3000g for 10 min at 4 °C, and the supernatant was collected and stored at −80 °C. The proteins levels of Aβ1-40 (27713, IBL), Aβ1-42 (27711, IBL), phospho-tau (pT181) (KHO0631, Invitrogen), and total-tau (KHB0041, Invitrogen) were measured by enzyme-linked immunosorbent assay (ELISA) according to manufacturer’s instructions. BCA analysis was performed with the same samples, and the data were normalized by the total protein content. Levels of Aβs secreted from E3^par and E4^iso iCOs were further measured using xMAP technology (Bioplex 200 systems). The utilized protocol is also described in our previous paper^{66 (link)}.

Park J.C., Jang S.Y., Lee D., Lee J., Kang U., Chang H., Kim H.J., Han S.H., Seo J., Choi M., Lee D.Y., Byun M.S., Yi D., Cho K.H, & Mook-Jung I. (2021). A logical network-based drug-screening platform for Alzheimer’s disease representing pathological features of human brain organoids. Nature Communications, 12, 280.

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Plasma Biomarker Panel in Lean Individuals

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Patients with BMI <25 kg/m² were chosen and the plasma were subjected to the following tests using commercially available kit: leptin (RAB0333, Millipore Sigma), glucose (TR15421, Thermo Fisher), cholesterol (MAK043, Sigma-Aldrich), triglyceride (10010303, Cayman), HDL (80059, Crystal Chem), Aβ₄₀ (KHB3481, Invitrogen), Aβ₄₂ (KHB3441, Invitrogen), p-Taul81 (KHO0631, Invitrogen). All tests were performed following standard protocols.

Tian J., Wang T., Jia K., Guo L., Swerdlow R.H, & Du H. (2022). Nonobese Male Patients with Alzheimer’s Disease Are Vulnerable to Decrease in Plasma Leptin. Journal of Alzheimer's disease : JAD, 88(3), 1017-1027.

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Amyloid-β Solubility and Tau Quantification

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Amyloid-β (Aβ) solubility was determined in soluble fractions from, (1) 0.2% diethylamine (DEA), (2) radioimmuniprecipitation assay buffer (RIPA), and (3) 70% formic acid (FA), using sequential isolation conditions, respectively, as previously described (Murphy et al, 2007; Niedowicz et al, 2013; 2014). Aβ was quantified with a sandwich ELISA, as previously described (Murphy et al, 2007; Niedowicz et al, 2013; 2014). Aβ40 and Aβ42 were measured in the DEA and RIPA fractions using commercially available kits (Invitrogen, KHB3481 and KHB3544, respectively), according to the manufacturer’s instructions. To detect total Aβ in the FA fraction, capture antibody Ab42.5 (against Aβ1-16; 0.5 μg / well) was used, followed by detection antibody: 0.25 μg/mL of biotinylated 4G8 (against Aβ17-24; BioLegend, San Diego, CA), as we had not previously tested the commercial kits using FA. Aβ levels were normalized to total protein concentrations loaded per well, as determined by bicinchoninic acid assay (Pierce). Phosphorylated tau pT181 (KHO0631) and total tau (KHB0041) was measured in the RIPA fraction (Invitrogen). Personnel performing the assays were blinded to mouse treatment condition.

Duncan M.J., Guerriero L.E., Kohler K., Beechem L.E., Gillis B.D., Salisbury F., Wessel C., Wang J., Sunderam S., Bachstetter A.D., O’Hara B.F, & Murphy M.P. (2021). Chronic fragmentation of the daily sleep-wake rhythm increases amyloid-beta levels and neuroinflammation in the 3xTg-AD mouse model of Alzheimer’s disease. Neuroscience, 481, 111-122.

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Blood Biomarkers for Alzheimer's Disease

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Amyloid-β and Tau-pT181 levels in blood specimens were measured using the enzyme-linked immunosorbent assay (ELISA) methods. The ELISA kits for Aβ₄₀ (KHB3481), Aβ₄₂ (KHB3441), and Tau-pT181 proteins (KHO0631) were obtained from Invitrogen (Carlsbad, CA, USA). All blood specimens were collected between 6:00 and 9:00 a.m. in a fasted state. Heparin anticoagulant blood was collected by a vacuum tube and centrifuged at 3000 rpm for 10 min for plasma separation. The samples were then aliquoted and stored at −80 °C. ELISA assays were conducted within one week at three repeats for each specimen.

Huang H., Li M., Zhang M., Qiu J., Cheng H., Mou X., Chen Q., Li T., Peng J, & Li B. (2021). Sleep Quality Improvement Enhances Neuropsychological Recovery and Reduces Blood Aβ42/40 Ratio in Patients with Mild–Moderate Cognitive Impairment. Medicina, 57(12), 1366.

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Quantification of Pathological Proteins in CSF

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The CSF levels of pathological proteins were determined using an enzyme-linked immunosorbent assay, including those of α-synuclein oligomer, Aβ_1-42, T-tau, and tau phosphorylated at the following positions: threonine 181 (P-tau_181t), threonine 231 (P-tau_231t), serine 396 (P-tau_396s), and serine 199 (P-tau_199s). CSB-E18033h, CSB-E10684h, and CSB-E12011h kits for measuring α-synuclein oligomer, Aβ_1-42, and T-tau, respectively, were obtained from CUSABIO (Wuhan, China), while KHB7031, KHB7041, KHB8051, and KHO0631 kits for measuring P-tau_396s, P-tau_199s, P-tau_231t, and P-tau_181t, respectively, were obtained from Invitrogen (Carlsbad, CA, USA). The levels of α-synuclein oligomer, Aβ_1-42, T-tau, P-tau_181t, P-tau_231t, P-tau_396s, and P-tau_199s were measured using a quantitative sandwich enzyme immunoassay.

Zuo L.J., Yu S.Y., Wang F., Hu Y., Piao Y.S., Du Y., Lian T.H., Wang R.D., Yu Q.J., Wang Y.J., Wang X.M., Chan P., Chen S.D., Wang Y, & Zhang W. (2016). Parkinson's Disease with Fatigue: Clinical Characteristics and Potential Mechanisms Relevant to α-Synuclein Oligomer. Journal of Clinical Neurology (Seoul, Korea), 12(2), 172-180.

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Solubilization and ELISA Analysis of EVs

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EVs were solubilized in guanidine hydrochloride buffer (8M Guanidine hydrochloride, 50mM Tris-HCl) supplemented with Halt™ Protease Inhibitor Cocktails and incubated at room temperature for 3 h with gentle agitation. After dilution of samples to 1:100 in dilution buffer, ELISAs were performed to assess levels of t-tau and p-tau (t-tau: # KHB0042 and pT181: # KHO0631, Thermo Fisher) according to manufacturer’s instructions.

Muraoka S., Lin W., Takamatsu-Yukawa K., Hu J., Ikezu S., DeTure M.A., Dickson D.W., Emili A, & Ikezu T. (2021). Enrichment of Phosphorylated Tau (Thr181) and Functionally Interacting Molecules in Chronic Traumatic Encephalopathy Brain-derived Extracellular Vesicles. Aging and Disease, 12(6), 1376-1388.

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Quantifying Tau Proteins in Brain and Nasal Tissues

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For ELISA analysis, brain and nasal tissues were homogenized in a 50-fold homogenization buffer (50 mM Tris HCL buffer, pH 8.0, 8 M guanidine HCl, 200 mM NaCl, 2 mM EDTA, and 0.05%n-dodecyl-β-d-maltoside for 1 min using a homogenizer (Physcotron NS-310E11; Microtec) and were stored at −80°C until use. The homogenates were thawed and mixed well, and then centrifuged at 14,000×g for 20 min at 25°C. Subsequently, the supernatants (90μl) were filtered with Sephadex G-10 (GE Healthcare Life Science) set in a Bio-Spin Chromatography Column (Bio-Rad Laboratories) by centrifugation at 800×g for 1 min at 25°C, to remove guanidine HCl. After the total protein concentration was determined using a Pierce BCA Protein Assay Kit (ThermoFisher Scientific), total tau (t-tau) and phosphorylated tau (pT181) were measured in triplicate using commercially available kits (KHB0042 and KHO0631, respectively; ThermoFisher Scientific), according to manufacturer’s instructions. Optical density at 450 nm in each well was measured using a microplate reader (Infinite M200; Tecan, Männedorf, Switzerland).

Pahrudin Arrozi A., Yanagisawa D., Kato T., Akatsu H., Hashizume Y., Kaneda D, & Tooyama I. (2021). Nasal Extracts from Patients with Alzheimer’s Disease Induce Tau Aggregates in a Cellular Model of Tau Propagation. Journal of Alzheimer's Disease Reports, 5(1), 263-274.

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