Evidence map›Paper›PMID 29596968›Full record

ReviewMolecular and cellular endocrinology2018

Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells:interactions of MAPK, MYC and glucocorticoid pathways.

M S Webb, A L Miller, T L Howard, B H Johnson, S Chumakov, Y Fofanov, T Nguyen-Vu, C Y Lin, E B Thompson

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular and cellular endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

9 authors at 3 institutions in 2 countries.

M S WebbDept. of Biochemistry & Molecular Biology, University of Texas Medical Branch, Galveston TX 77555, USA.
A L MillerDept. of Biochemistry & Molecular Biology, University of Texas Medical Branch, Galveston TX 77555, USA.
T L HowardDept. of Biochemistry & Molecular Biology, University of Texas Medical Branch, Galveston TX 77555, USA.
B H JohnsonDept. of Biochemistry & Molecular Biology, University of Texas Medical Branch, Galveston TX 77555, USA.
S ChumakovDept. of Computer Science, Dept. of Physics, University of Guadalahara, Gaudalahara, Jalisco, Mexico.
Y FofanovDept. of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston TX 77555, USA.
T Nguyen-VuCenter for Nuclear Receptors & Cell Signaling, Dept. of Biology & Biochemistry, University of Houston, Houston TX 77204, USA.
C Y LinCenter for Nuclear Receptors & Cell Signaling, Dept. of Biology & Biochemistry, University of Houston, Houston TX 77204, USA.
E B ThompsonDept. of Biochemistry & Molecular Biology, University of Texas Medical Branch, Galveston TX 77555, USA; Center for Nuclear Receptors & Cell Signaling, Dept. of Biology & Biochemistry, University of Houston, Houston TX 77204, USA. Electronic address: bthompso@utmb.edu.
The University of Texas Medical Branch at Galveston · USUniversity of Houston · USSecretaría de Salud de Jalisco · MX

Funding

THE HUMAN GLUCOCORTICOID RECEPTORS, ITS GENE AND ACTIONSR01CA041407 · NCI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI THOMPSON, E B · 1986 to 2006
$1.6M
NCI NIH HHS R01 CA041407
6 · The paper itself

Abstract

Gene expression responses to glucocorticoid (GC) in the hours preceding onset of apoptosis were compared in three clones of human acute lymphoblastic leukemia CEM cells. Between 2 and 20h, all three clones showed increasing numbers of responding genes. Each clone had many unique responses, but the two responsive clones showed a group of responding genes in common, different from the resistant clone. MYC levels and the balance of activities between the three major groups of MAPKs are known important regulators of glucocorticoid-driven apoptosis in several lymphoid cell systems. Common to the two sensitive clones were changed transcript levels from genes that decrease amounts or activity of anti-apoptotic ERK/MAPK1 and JNK2/MAPK9, or of genes that increase activity of pro-apoptotic p38/MAPK14. Down-regulation of MYC and several MYC-regulated genes relevant to MAPKs also occurred in both sensitive clones. Transcriptomine comparisons revealed probable NOTCH-GC crosstalk in these cells.

Indexed as

Signal TransductionApoptosisCalcineurinCell Line, TumorDexamethasoneGene Expression Regulation, LeukemicGene Regulatory NetworksGlucocorticoidsHumansLeukemiaMitogen-Activated Protein KinasesProto-Oncogene Proteins c-mycReceptors, NotchReproducibility of ResultsTime FactorsTranscriptomeCalcineurinDexamethasoneGlucocorticoidsMitogen-Activated Protein KinasesProto-Oncogene Proteins c-mycReceptors, Notch

Identifiers

PMID29596968
PMCPMC6075652
OpenAlexW2790534376

What OpenQuestion holds

Textmetadata
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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.