CLU Knockout Cell Lysate

Name: CLU Knockout Cell Lysate
SKU: DAG-KO131
Rating: 5 (1 reviews)

CLU Knockout Cell Lysate from HeLa cell line for anti-CLU antibody specificity validation.

COA

SDS

Datasheet

Summary

Product Overview

HeLa cell lines were engineered into double-knockout lines by CRISPR technology. The double knockout genotype was verified by PCR followed by sequencing. The CLU knockout cell lysate are the cell homogenate in RIPA buffer made from the KO cell lines. A vial of lysate from the parental cell line was also provided as an internal control.

Nature

Cell Lysate

Alternative Names

CLU; clusterin; CLI; AAG4; APOJ; CLU1; CLU2; KUB1; SGP2; APO-J; SGP-2; SP-40; TRPM2; TRPM-2; NA1/NA2; apolipoprotein J; ku70-binding protein 1; sulfated glycoprotein 2; aging-associated protein 4; complement lysis inhibitor; complement cytolysis inhibitor; complement-associated protein SP-40,40; testosterone-repressed prostate message 2;

Application Notes

Prior to SDS-PAGE fractionation, boil the lysate for 5 minutes.

Dilution

Lysate samples can be diluted with 2x SDS Sample Buffer.
After dilution, the protein sample should be aliquoted and stored at -20°C for long term storage.

Format

Lyophilized

Concentration

The protein concentration was determined with BCA assay.

Buffer

RIPA buffer

Preservative

None

Storage

Store at -20°C. Avoid repeated freeze-thaw cycles.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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Customer Reviews

References

Plasma A beta(42) as a Biomarker of Prodromal Alzheimer's Disease Progression in Patients with Amnestic Mild Cognitive Impairment: Evidence from the PharmaCog/E-ADNI Study

JOURNAL OF ALZHEIMERS DISEASE

Authors: Albani, Diego; Marizzoni, Moira; Ferrari, Clarissa; Fusco, Federica; Boeri, Lucia; Raimondi, Ilaria; Jovicich, Jorge; Babiloni, Claudio; Soricelli, Andrea; Lizio, Roberta; Galluzzi, Samantha; Cavaliere, Libera; Didic, Mira; Schoenknecht, Peter; Luis Molinuevo, Jose; Nobili, Flavio; Parnetti, Lucilla; Payoux, Pierre; Bocchio, Luisella; Salvatore, Marco; Rossini, Paolo Maria; Tsolaki, Magda; Visser, Pieter Jelle; Richardson, Jill C.; Wiltfang, Jens; Bordet, Regis; Blin, Olivier; Forloni, Gianluigi; Frisoni, Giovanni B.

Abstract

It is an open issue whether blood biomarkers serve to diagnose Alzheimer's disease (AD) or monitor its progression over time from prodromal stages. Here, we addressed this question starting from data of the European FP7 IMI-PharmaCog/E-ADNI longitudinal study in amnesic mild cognitive impairment (aMCI) patients including biological, clinical, neuropsychological (e.g., ADAS-Cog13), neuroimaging, and electroencephalographic measures. PharmaCog/E-ADNI patients were classified as "positive" (i.e., "prodromal AD"; n = 76) or "negative" (n = 52) based on a diagnostic cut-off of A beta(42)/P-tau in cerebrospinal fluid as well as APOE epsilon 4 genotype. Blood was sampled at baseline and at two followups (12 and 18 months), when plasma amyloid peptide 42 and 40 (A beta(42), A beta(40)) and apolipoprotein J (clusterin, CLU) were assessed. Linear Mixed Models found no significant differences in plasma molecules between the "positive" (i. e., prodromal AD) and "negative" groups at baseline. In contrast, plasma A beta(42) showed a greater reduction over time in the prodromal AD than the "negative" aMCI group (p = 0.048), while CLU and A beta(40) increased, but similarly in the two groups. Furthermore, plasma A beta(42) correlated with the ADAS-Cog13 score both in aMCI patients as a whole and the prodromal AD group alone. Finally, CLU correlated with the ADAS-Cog13 only in the whole aMCI group, and no association with ADAS-Cog13 was found for A beta(40). In conclusion, plasma A beta(42) showed disease progression-related features in aMCI patients with prodromal AD.

Risk-reducing Apolipoprotein E and Clusterin genotypes protect against the consequences of poor vascular health on executive function performance and change in nondemented older adults

NEUROBIOLOGY OF AGING

Authors: McFall, G. Peggy; Sapkota, Shraddha; McDermott, Kirstie L.; Dixon, Roger A.

Abstract

We examined independent and cumulative effects of 2 Alzheimer's-related genetic polymorphisms, Apolipoprotein E (APOE) and Clusterin (CLU), in relation to the deleterious effects of poor vascular health (pulse pressure [PP]) on executive function (EF) performance and change in nondemented older adults. Using a sample (n = 593; age range = 53-95 years) from the Victoria Longitudinal Study, we applied latent growth modeling to test the effect of PP, as moderated by APOE and CLU, on an EF latent variable. EF was affected by higher levels of PP but differentially less so for carriers of low-risk alleles (APOE epsilon 2+; CLU TT) than for moderate-or high-risk alleles (APOE epsilon 2+; CLU C+). The cumulative genetic risk of APOE plus CLU provided similar moderation of PP level effects on EF. Future research may focus on how APOE and CLU might provide different but complementary contributions to predicting EF level and change. Vascular health risk in synergistic association with risk-related polymorphisms can elucidate the neurobiological underpinnings of cognitive trajectories in nondemented aging. (C) 2016 Elsevier Inc. All rights reserved.