Evidence map›Paper›PMID 19707560›Full record

ArticlePloS one2009

New Alzheimer amyloid beta responsive genes identified in human neuroblastoma cells by hierarchical clustering.

Markus Uhrig, Carina Ittrich, Verena Wiedmann, Yuri Knyazev, Annette Weninger, Matthias Riemenschneider, Tobias Hartmann

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Copy number loss Of APP cause thoracic aortic dissection.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
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  4. 1,25(OH)International journal of molecular sciences · 2020
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  12. Characterization of multiple exon 1 variants in mammalian HuD mRNA and neuron-specific transcriptional control via neurogenin 2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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 3 institutions in 1 country.

Markus UhrigCenter for Molecular Biology of the University of Heidelberg (ZMBH), Heidelberg, Germany.
Carina Ittrich
Verena Wiedmann
Yuri Knyazev
Annette Weninger
Matthias Riemenschneider
Tobias Hartmann
Heidelberg University · DESaarland University · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by neuronal degeneration and cell loss. Abeta(42), in contrast to Abeta(40), is thought to be the pathogenic form triggering the pathological cascade in AD. In order to unravel overall gene regulation we monitored the transcriptomic responses to increased or decreased Abeta(40) and Abeta(42) levels, generated and derived from its precursor C99 (C-terminal fragment of APP comprising 99 amino acids) in human neuroblastoma cells. We identified fourteen differentially expressed transcripts by hierarchical clustering and discussed their involvement in AD. These fourteen transcripts were grouped into two main clusters each showing distinct differential expression patterns depending on Abeta(40) and Abeta(42) levels. Among these transcripts we discovered an unexpected inverse and strong differential expression of neurogenin 2 (NEUROG2) and KIAA0125 in all examined cell clones. C99-overexpression had a similar effect on NEUROG2 and KIAA0125 expression as a decreased Abeta(42)/Abeta(40) ratio. Importantly however, an increased Abeta(42)/Abeta(40) ratio, which is typical of AD, had an inverse expression pattern of NEUROG2 and KIAA0125: An increased Abeta(42)/Abeta(40) ratio up-regulated NEUROG2, but down-regulated KIAA0125, whereas the opposite regulation pattern was observed for a decreased Abeta(42)/Abeta(40) ratio. We discuss the possibilities that the so far uncharacterized KIAA0125 might be a counter player of NEUROG2 and that KIAA0125 could be involved in neurogenesis, due to the involvement of NEUROG2 in developmental neural processes.

Indexed as

Amyloid beta-PeptidesBasic Helix-Loop-Helix ProteinsCell Line, TumorCluster AnalysisEnzyme-Linked Immunosorbent AssayHumansNerve Tissue ProteinsNeuroblastomaPolymerase Chain ReactionAmyloid beta-PeptidesBasic Helix-Loop-Helix ProteinsNerve Tissue ProteinsNEUROG2 protein, human

Identifiers

PMID19707560
PMCPMC2727959
OpenAlexW1981274981

What OpenQuestion holds

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LicenceCC BY
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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.