Evidence map›Paper›PMID 32111982›Full record

ArticleOncogene2020

Hypoxia and the hypoxia inducible factor 1α activate protein kinase A by repressing RII beta subunit transcription.

Kristin Lucia, Yonghe Wu, Jose Monteserin Garcia, Anne Barlier, Michael Buchfelder, Wolfgang Saeger, Ulrich Renner, Günter K Stalla, Marily Theodoropoulou

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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  15. Single-cell analysis of myeloid cells in HPVFrontiers in immunology · 2022
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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

9 authors at 6 institutions in 2 countries.

Kristin LuciaDepartment of Endocrinology, Max Planck Institute of Psychiatry, Munich, Germany.
Yonghe WuDivision of Molecular Genetics, Deutsches Krebsforschungszentrum, Heidelberg, Germany.
Jose Monteserin GarciaDepartment of Endocrinology, Max Planck Institute of Psychiatry, Munich, Germany.
Anne BarlierCentre de Recherche en Neurobiologie et Neurophysiologie de Marseille, Marseille, France.
Michael BuchfelderDepartment of Neurosurgery, Klinikum der Universität Erlangen, Erlangen, Germany.
Wolfgang SaegerDepartment of Neuropathology, Universität Hamburg, Hamburg, Germany.
Ulrich RennerDepartment of Endocrinology, Max Planck Institute of Psychiatry, Munich, Germany.
Günter K StallaDepartment of Endocrinology, Max Planck Institute of Psychiatry, Munich, Germany.
Marily TheodoropoulouDepartment of Endocrinology, Max Planck Institute of Psychiatry, Munich, Germany. marily.theodoropoulou@med.uni-muechen.de.
Max Planck Institute of Psychiatry · DELudwig-Maximilians-Universität München · DECentre de Recherche en Neurobiologie - Neurophysiologie de Marseille · FRGerman Cancer Research Center · DEUniversität Hamburg · DEUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overactivation of the cAMP signal transduction pathway plays a central role in the pathogenesis of endocrine tumors. Genetic aberrations leading to increased intracellular cAMP or directly affecting PKA subunit expression have been identified in inherited and sporadic endocrine tumors, but are rare indicating the presence of nongenomic pathological PKA activation. In the present study, we examined the impact of hypoxia on PKA activation using human growth hormone (GH)-secreting pituitary tumors as a model of an endocrine disease displaying PKA-CREB overactivation. We show that hypoxia activates PKA and enhances CREB transcriptional activity and subsequently GH oversecretion. This is due to a previously uncharacterized ability of HIF-1α to suppress the transcription of the PKA regulatory subunit 2B (PRKAR2B) by sequestering Sp1 from the PRKAR2B promoter. The present study reveals a novel mechanism through which the transcription factor HIF-1α transduces environmental signals directly onto PKA activity, without affecting intracellular cAMP concentrations. By identifying a point of interaction between the cellular microenvironment and intracellular enzyme activation, neoplastic, and nonneoplastic diseases involving overactivated PKA pathway may be more efficiently targeted.

Indexed as

Cell Line, TumorCyclic AMP-Dependent Protein Kinase RIIalpha SubunitCyclic AMP-Dependent Protein Kinase RIIbeta SubunitGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitImmunoglobulinsPhosphorylationPituitary NeoplasmsSignal TransductionTranscriptional ActivationTumor HypoxiaCyclic AMP-Dependent Protein Kinase RIIalpha SubunitCyclic AMP-Dependent Protein Kinase RIIbeta SubunitHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitImmunoglobulinsPRKAR2A protein, humanPRKAR2B protein, humanSP1 antigen

Identifiers

PMID32111982
PMCPMC7160059
OpenAlexW3007429206

What OpenQuestion holds

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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.