Evidence map›Paper›PMID 23959845›Full record

ReviewJournal of cellular biochemistry2014

Eliminative signaling by Janus kinases: role in the downregulation of associated receptors.

Christopher J Carbone, Serge Y Fuchs

Abstract readReview
In one paragraph

Review in Journal of cellular biochemistry, 2014. 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 35% 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, 7 citations in OpenAlex.

  1. Article
  2. Aberrantly low STAT3 and STAT5 responses are associated with poor outcome and an inflammatory gene expression signature in pediatric acute myeloid leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  3. Review
  4. A PotentClinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  5. Molecular targets of luteolin in cancer.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2016
    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

2 authors at 1 institution in 1 country.

Christopher J CarboneDepartment of Animal Biology and Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, 19104.
Serge Y Fuchs
University of Pennsylvania · US

Funding

Role of HOS in Cell Transformation and ApoptosisR01CA092900 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2001 to 2021
$5.3M
Interferon Responses in Myeloid LeukemiaR01CA142425 · NCI · UNIVERSITY OF PENNSYLVANIA · PI FUCHS, SERGE Y · 2010 to 2014
$1.6M
NCI NIH HHS CA092900NCI NIH HHS CA142425NCI NIH HHS R01 CA092900NCI NIH HHS R01 CA142425
6 · The paper itself

Abstract

Activation of cytokine receptor-associated Janus kinases (JAKs) mediates most, if not all, of the cellular responses to peptide hormones and cytokines. Consequently, JAKs play a paramount role in homeostasis and immunity. Members of this family of tyrosine kinases control the cytokine/hormone-induced alterations in cell gene expression program. This function is largely mediated through an ability to signal toward activation of the signal transducer and activator of transcription proteins (STAT), as well as toward some other pathways. Importantly, JAKs are also instrumental in tightly controlling the expression of associated cytokine and hormone receptors, and, accordingly, in regulating the cell sensitivity to these cytokines and hormones. This review highlights the enzymatic and non-enzymatic mechanisms of this regulation and discusses the importance of the ambidextrous nature of JAK as a key signaling node that integrates the combining functions of forward signaling and eliminative signaling. Attention to the latter aspect of JAK function may contribute to emancipating our approaches to the pharmacological modulation of JAKs.

Indexed as

Signal TransductionAnimalsCytokinesHumansJanus KinasesMolecular Targeted TherapyReceptors, ErythropoietinReceptors, InterferonReceptors, ProlactinReceptors, ThrombopoietinCytokinesJanus KinasesReceptors, ErythropoietinReceptors, InterferonReceptors, ProlactinReceptors, ThrombopoietinCYTOKINEDOWNREGULATIONJAKKINASERECEPTOR

Identifiers

PMID23959845
PMCPMC3856693
OpenAlexW1935067082

What OpenQuestion holds

Textmetadata
LicenceTDM
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.