Evidence map›Paper›PMID 29382715›Full record

ArticleThe Journal of biological chemistry2018

Stat3 and CCAAT enhancer-binding protein β (C/ebpβ) activate Fanconi C gene transcription during emergency granulopoiesis.

Chirag A Shah, Larisa Broglie, Liping Hu, Ling Bei, Weiqi Huang, Danielle B Dressler, Elizabeth A Eklund

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Human DNA methylation signatures differentiate persistent from resolving MRSA bacteremia.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  4. Review
  5. Review
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

7 authors at 3 institutions in 1 country.

Chirag A ShahFrom the Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60605.
Larisa Brogliethe Children's Hospital of Wisconsin, Medical College of Wisconsin, Milwaukee, Wisconsin 53213.
Liping HuFrom the Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60605.
Ling BeiFrom the Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60605.
Weiqi HuangFrom the Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60605.
Danielle B DresslerFrom the Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60605.
Elizabeth A EklundFrom the Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60605, e-eklund@northwestern.edu.
Northwestern University · USJesse Brown VA Medical Center · USChildren's Hospital of Wisconsin · US

Funding

The role of ICSBP in the pathogenesis of chronic myeloid leukemiaR01CA174205 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI EKLUND, ELIZABETH ANN · 2013 to 2017
$1.6M
Molecular mechanisms for bone marrow failure and clonal progression during the innate immune response in Fanconi AnemiaR01DK121354 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI EKLUND, ELIZABETH ANN · 2019 to 2022
$1.4M
The role of emergency granulopoiesis in the pathogenesis of Fanconi AnemiaR01DK098812 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI EKLUND, ELIZABETH ANN · 2014 to 2017
$1.3M
Molecular Mechanisms of Disease Progression in Myeloid MalignancyI01BX002067 · VA · JESSE BROWN VA MEDICAL CENTER · PI EKLUND, ELIZABETH ANN · 2013 to 2016
–
Molecular mechanisms of drug resistance and disease progression in acute myeloid leukemia.I01BX004635 · VA · JESSE BROWN VA MEDICAL CENTER · PI EKLUND, ELIZABETH ANN · 2019 to 2025
–
Identifying molecular markers that predict relapse after therapy discontinuation inchronic myeloid leukemia.I01CX001864 · VA · JESSE BROWN VA MEDICAL CENTER · PI Elizabeth Ann Eklund · 2019 to 2026
–
BLRD VA I01 BX002067BLRD VA I01 BX004635CSRD VA I01 CX001864NCI NIH HHS R01 CA174205NIDDK NIH HHS R01 DK098812NIDDK NIH HHS R01 DK121354
6 · The paper itself

Abstract

Interferon consensus sequence-binding protein (Icsbp) is required for terminating emergency granulopoiesis, an episodic event responsible for granulocyte production in response to infections and a key component of the innate immune response. Icsbp inhibits the expression of Stat3 and C/ebpβ, transcription factors essential for initiating and sustaining granulopoiesis, and activates transcription of Fanconi C (

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsApoptosisBase SequenceCCAAT-Enhancer-Binding Protein-betaDNA RepairFanconi Anemia Complementation Group C ProteinGranulocytesHematopoiesisHumansMiceMice, Inbred C57BLPromoter Regions, GeneticSequence HomologySTAT3 Transcription FactorCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanCebpb protein, mouseFanconi Anemia Complementation Group C ProteinSTAT3 Transcription FactorCCAAT-enhancer-binding protein (C/EBP)DNA repairinnate immunityStat3STAT transcription factorstress response

Identifiers

PMID29382715
PMCPMC5857980
OpenAlexW2785524682

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.