Evidence map›Paper›PMID 38727904›Full record

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

Generation of Rare Human NMDA Receptor Variants in Mice.

Rolf Sprengel, Ahmed Eltokhi, Frank N Single

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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Rolf SprengelMax Planck Institute for Medical Research, Heidelberg, Germany. sprengel@mr.mpg.de.
Ahmed EltokhiDepartment of Biomedical Sciences, School of Medicine, Mercer University, Columbus, GA, USA.
Frank N SingleMiltenyi Biotec B.V. & Co. KG, Bergisch Gladbach, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The analysis of rare NMDAR gene variants in mice, coupled with a fundamental understanding of NMDAR function, plays a crucial role in achieving therapeutic success when addressing NMDAR dysfunctions in human patients. For the generation of such NMDAR mouse models, a basic knowledge of receptor structure, along with skills in database sequence analysis, cloning in E. coli, genetic manipulation of embryonic stem (ES) cells, and ultimately the genetic modification of mouse embryos, is essential. Primarily, this chapter will focus on the design and synthesis of NMDAR gene-targeting vectors that can be used successfully for the genetic manipulation of mice. We will outline the core principles of the design and synthesis of a gene targeting vector that facilitates the introduction of single-point mutations in NMDAR-encoding genes in mice. The transformation of ES cells, selection of positive ES cell colonies, manipulation of mouse embryos, and genotyping strategies will be described briefly.

Indexed as

Receptors, N-Methyl-D-AspartateAnimalsEmbryonic Stem CellsGene TargetingGenetic VectorsHumansMiceReceptors, N-Methyl-D-AspartateConditional and global NMDAR mutant miceGene-targeted miceGene-targeting vectorsHypomorphic allele

Identifiers

PMID38727904

What OpenQuestion holds

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Registered trials

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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.