Evidence map›Paper›PMID 38512673›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2024

Western Blot of Tau Protein from Mouse Brains Extracts: How to Avoid Signal Artifacts.

Parissa Fereydouni-Forouzandeh, Geoffrey Canet, Sofia Diego-Diàz, Emma Rocaboy, Serena Petry, Robert A Whittington, Emmanuel Planel

Abstract read
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In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
4.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Parissa Fereydouni-Forouzandeh *Université Laval, Faculté de Médecine, Département de Psychiatrie et Neurosciences, Quebec, QC, Canada.
Geoffrey Canet *Université Laval, Faculté de Médecine, Département de Psychiatrie et Neurosciences, Quebec, QC, Canada.
Sofia Diego-DiàzUniversité Laval, Faculté de Médecine, Département de Psychiatrie et Neurosciences, Quebec, QC, Canada.
Emma RocaboyUniversité Laval, Faculté de Médecine, Département de Psychiatrie et Neurosciences, Quebec, QC, Canada.
Serena PetryUniversité Laval, Faculté de Médecine, Département de Psychiatrie et Neurosciences, Quebec, QC, Canada.
Robert A WhittingtonDepartment of Anesthesiology and Perioperative Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Emmanuel PlanelUniversité Laval, Faculté de Médecine, Département de Psychiatrie et Neurosciences, Quebec, QC, Canada. emmanuel.planel@neurosciences.ulaval.ca.
Université Laval · CAUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tau is a microtubule-associated protein enriched in the axonal compartment. Its most well-known function is to bind and stabilize microtubules. In Alzheimer's disease and other neurodegenerative diseases known as tauopathies, tau undergoes several abnormal post-translational modifications including hyperphosphorylation, conformational changes, oligomerization, and aggregation. Numerous mouse models of tauopathies have been developed, and Western blotting remains an invaluable tool in studying tau protein physiological and pathological changes in these models. However, many of the antibodies that have been developed to analyze tau post-translational modifications are mouse monoclonal, which are at risk of producing artifactual signals in Western blotting procedures. This risk does not arise due to their lack of specificity, but rather because the secondary antibodies used to detect them will also react with the heavy chain of endogenous mouse immunoglobulins (Igs), leading to a non-specific signal at the same molecular weight as tau protein (around 50 kDa). Here, we present the use of anti-light-chain secondary antibodies as a simple and efficient technique to prevent non-specific Ig signals around 50 kDa. We demonstrate the efficacy of this method by either eliminating or identifying artifactual signals when using monoclonal antibodies directed at non-phosphorylated epitopes (T49, Tau3R, Tau4R), phosphorylated epitopes (MC6, AT180, CP13), or an abnormal tau conformation (MC1), in wild-type (WT) mice with tau hyperphosphorylation (hypothermic), transgenic mice overexpressing human tau (hTau mice), and tau knockout (TKO) mice.

Indexed as

Alzheimer DiseaseTauopathiesAnimalsArtifactsBlotting, WesternBrainEpitopesHumansMiceMice, KnockoutMice, TransgenicPhosphorylationtau ProteinsEpitopestau ProteinsAlzheimer’s diseaseAntibody specificityLight-chain antibodyMouse modelsTau phosphorylation

Identifiers

PMID38512673
OpenAlexW4393061742

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.