Evidence map›Paper›PMID 23872956›Full record

ArticleCellular and molecular life sciences : CMLS2014

The HIF-1 transcription complex is essential for translational control of myeloid hematopoietic cell function by maintaining mTOR phosphorylation.

Inna M Yasinska, Bernhard F Gibbs, Gurprit S Lall, Vadim V Sumbayev

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  4. mTORC1 is required for expression of LRPPRC and cytochrome-American journal of physiology. Cell physiology · 2019
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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

4 authors at 2 institutions in 1 country.

Inna M YasinskaMedway School of Pharmacy, University of Kent, Anson Building, Central Avenue, Chatham Maritime, Kent, ME4 4TB, UK.
Bernhard F Gibbs
Gurprit S Lall
Vadim V Sumbayev
University of Kent · GBMedway School of Pharmacy · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian myeloid cells are crucial effectors of host innate immune defense. Normal and pathological responses of these cells require adaptation to signaling stress through the hypoxia-inducible factor 1 (HIF-1) transcription complex. Adapted cells activate the mammalian target of rapamycin (mTOR), via S2448 phosphorylation, which induces de novo translation of vital signaling proteins. However, the molecular mechanisms underlying this signaling dogma remain unclear. Here, we demonstrate for the first time that inactivation of HIF-1, by silencing its inducible alpha subunit, significantly decreases mTOR S2448 phosphorylation caused by ligand-dependent activation of human myeloid leukemia cells. This shows that HIF-1 is essential for the activation of mTOR and serves at a crucial juncture of myeloid cell function in both in vitro and in vivo systems.

Indexed as

AMP-Activated Protein KinasesAnimalsBlood CellsCell LineEnzyme ActivationHumansHypoxia-Inducible Factor 1MaleMiceMyeloid CellsPhosphorylationRNA InterferenceRNA, Small InterferingToll-Like Receptor 2TOR Serine-Threonine KinasesAMP-Activated Protein KinasesHypoxia-Inducible Factor 1RNA, Small InterferingTlr2 protein, mouseToll-Like Receptor 2TOR Serine-Threonine Kinases

Identifiers

PMID23872956
PMCPMC11113144
OpenAlexW2007090162

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.