Evidence map›Paper›PMID 21562815›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2011

Learning about the functions of NME/NM23: lessons from knockout mice to silencing strategies.

Mathieu Boissan, Marie-Lise Lacombe

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. NME/NM23/NDPK and Histidine Phosphorylation.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Article
  10. Frontiers in microbiology · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The dosage-dependent effect exerted by the NM23-H1/H2 homolog NDK-1 on distal tip cell migration in C. elegans.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  16. Histidine kinases and the missing phosphoproteome from prokaryotes to eukaryotes.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  17. The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  18. Article
  19. Nucleoside diphosphate kinases (NDPKs) in animal development.Cellular and molecular life sciences : CMLS · 2015
    Review
  20. 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

2 authors at 2 institutions in 1 country.

Mathieu BoissanUPMC Université Paris 06, 75005, Paris, France. mathieu.boissan@inserm.fr
Marie-Lise Lacombe
Inserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human NME gene family (also known as NM23) comprises ten genes that are involved in diverse physiological and pathological processes including proliferation, differentiation, development, ciliary functions, and metastasis. For the moment, only the NME1, NME2, and NME7 genes have been inactivated in transgenic knockout mice, as well as a double NME1-NME2 gene knockout. Mice lacking NME1 or NME2 grow to adulthood without health problems, although NME1 (-/-) mice have modest growth retardation. Double knockout NME1 (-/-)-NME2 (-/-) mice, by contrast, are highly hypotrophic and die at birth from profound anemia due to impaired erythroblast development. Evidence for a metastasis suppressor function of NME1 in vivo comes from crossing NME1 (-/-) mice with mice prone to develop hepatocellular carcinoma; the double transgenic mice present a higher incidence of lung metastases. Silencing of NME1 by siRNA interference has confirmed this function by conferring a "metastatic phenotype" on non-invasive human epithelial cancer cell lines. This function is specific to NME1 and is not observed when the NME2 is silenced. The data indicate that NME1 loss is causally involved at the early stages of the metastatic cascade. NME2 (-/-) mice and NME2 silencing experiments reveal a specific role of NME2 in activation of heterotrimeric G proteins and of KCa3.1 channel in T cells, pointing to a role of NME2 as a histidine phosphotransferase. Regarding NME7, consistent with its expression in axonemal structures, NME7 (-/-) mice present lesions similar to primary ciliary dyskinesia. This review summarizes the recent data obtained by knockout and silencing of NME/NM23 genes that provide mechanistic insights into their respective roles in physiology and pathology.

Indexed as

Gene SilencingModels, GeneticAnimalsCell Line, TumorHumansMiceMice, KnockoutNeoplasm MetastasisNeoplasmsNM23 Nucleoside Diphosphate KinasesProtein SubunitsNM23 Nucleoside Diphosphate KinasesProtein Subunits

Identifiers

PMID21562815
OpenAlexW2059721712

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.