Evidence map›Paper›PMID 26270350›Full record

ArticleCell death & disease2015

AK2 deficiency compromises the mitochondrial energy metabolism required for differentiation of human neutrophil and lymphoid lineages.

E Six, C Lagresle-Peyrou, S Susini, C De Chappedelaine, N Sigrist, H Sadek, M Chouteau, N Cagnard, M Fontenay, O Hermine and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

54 citing papers in PubMed, 88 citations in OpenAlex.

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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

16 authors at 3 institutions in 1 country.

E Six1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France.
C Lagresle-Peyrou1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France.
S Susini1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France.
C De Chappedelaine1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France.
N Sigrist1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France.
H Sadek1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France.
M Chouteau1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France.
N CagnardSFR Necker, Plateforme de bioinformatique, Paris Descartes-Sorbonne Paris Cité University, Paris, France.
M FontenayDepartment of Immunology and Hematology, Cochin Institute, INSERM U1016, Paris, France.
O Hermine1] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France [2] Department of Adult Hematology, Necker Children's Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.
C Chomienne1] Service de Biologie Cellulaire, Hopital Saint-Louis, Assistance Publique-Hôpitaux de Paris, Paris, France [2] INSERM UMRS 940, Diderot - Sorbonne Paris Cité University, Paris, France.
P ReynierUMR CNRS6214, INSERM 1083, Département de Biochimie et Génétique, Centre Hospitalier Universitaire, Angers, France.
A Fischer1] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France [2] Pediatric Immunology-Hematology and Rhumatology Department, Necker Children's Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France [3] Collège de France, Paris, France.
I André-Schmutz1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France.
N GueguenUMR CNRS6214, INSERM 1083, Département de Biochimie et Génétique, Centre Hospitalier Universitaire, Angers, France.
M Cavazzana1] Laboratory of Human Lymphohematopoiesis, INSERM UMR 1163, Paris, France [2] Paris Descartes-Sorbonne Paris Cité University, Imagine Institute, Paris, France [3] Biotherapy Department, Necker Children's Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France [4] Biotherapy Clinical Investigation Center, Groupe Hospitalier Universitaire Ouest, Assistance Publique-Hôpitaux de Paris, INSERM, Paris, France.
Délégation Paris 5 · FRCentre National de la Recherche Scientifique · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reticular dysgenesis is a human severe combined immunodeficiency that is primarily characterized by profound neutropenia and lymphopenia. The condition is caused by mutations in the adenylate kinase 2 (AK2) gene, resulting in the loss of mitochondrial AK2 protein expression. AK2 regulates the homeostasis of mitochondrial adenine nucleotides (ADP, ATP and AMP) by catalyzing the transfer of high-energy phosphate. Our present results demonstrate that AK2-knocked-down progenitor cells have poor proliferative and survival capacities and are blocked in their differentiation toward lymphoid and granulocyte lineages. We also observed that AK2 deficiency impaired mitochondrial function in general and oxidative phosphorylation in particular - showing that AK2 is critical in the control of energy metabolism. Loss of AK2 disrupts this regulation and leads to a profound block in lymphoid and myeloid cell differentiation.

Indexed as

Adenine NucleotidesAdenylate KinaseAntigens, CD34Cell DifferentiationGene Expression ProfilingGene Expression RegulationGene Knockdown TechniquesHL-60 CellsHumansLeukopeniaLymphocytesMitochondriaMutationNeutrophilsOxidative PhosphorylationPrimary Cell CultureAdenine NucleotidesAdenylate Kinaseadenylate kinase 2Antigens, CD34

Identifiers

PMID26270350
PMCPMC4558504
OpenAlexW1755717066

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.