Evidence map›Paper›PMID 25205818›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2014

Differential effects of STAT proteins on growth hormone-mediated IGF-I gene expression.

Ben Varco-Merth, Peter Rotwein

Abstract readComparative Study
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. STAT5B deficiency: Impacts on human growth and immunity.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2016
    Review
  11. Article
  12. 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

2 authors at 1 institution in 1 country.

Ben Varco-MerthDepartment of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, Oregon.
Peter RotweinDepartment of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, Oregon rotweinp@ohsu.edu.
Oregon Health & Science University · US

Funding

MULTIDISCIPLINARY TRAINING IN NEUROENDOCRINOLOGYT32DK007680 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI GOODMAN, RICHARD H. · 1991 to 2015
$6.8M
Control of IGF-1 Gene Transcription by Growth HormoneR01DK069703 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI ROTWEIN, PETER S · 2006 to 2014
$2.8M
NIDDK NIH HHS R01 DK069703NIDDK NIH HHS R01-DK-069703NIDDK NIH HHS T32 DK007680
6 · The paper itself

Abstract

Growth hormone (GH) plays a key role regulating somatic growth and in controlling metabolism and other physiological processes in humans and other animal species. GH acts by binding to the extracellular part of its transmembrane receptor, leading to induction of multiple intracellular signal transduction pathways that culminate in changes in gene and protein expression. A key agent in GH-stimulated growth is the latent transcription factor signal transducer and activator of transcription (STAT) 5B, one of four STAT proteins induced by the GH receptor in cultured cells and in vivo. As shown by genetic and biochemical studies, GH-activated STAT5B promotes transcription of the gene encoding the critical growth peptide, insulin-like growth factor-I (IGF-I), and natural null mutations of STAT5B in humans lead to growth failure accompanied by diminished IGF-I expression. Here we have examined the possibility that other GH-activated STATs can enhance IGF-I gene transcription, and thus potentially contribute to GH-regulated somatic growth. We find that human STAT5A is nearly identical to STAT5B in its biochemical and functional responses to GH but that STAT1 and STAT3 show a weaker profile of in vitro binding to STAT DNA elements from the IGF-I gene than STAT5B, and are less potent inducers of gene transcription through these elements. Taken together, our results offer a molecular explanation for why STAT5B is a key in vivo mediator of GH-activated IGF-I gene transcription and thus of GH-regulated somatic growth.

Indexed as

Up-RegulationAnimalsBase SequenceCell NucleusChlorocebus aethiopsConserved SequenceCOS CellsGrowth HormoneHumansInsulin-Like Growth Factor IPhosphorylationProtein Processing, Post-TranslationalProtein TransportRatsRecombinant Fusion ProteinsRecombinant ProteinsGrowth HormoneInsulin-Like Growth Factor IRecombinant Fusion ProteinsRecombinant ProteinsSTAT1 protein, humanSTAT1 Transcription FactorSTAT3 protein, humanSTAT3 Transcription FactorSTAT5A protein, humanSTAT5B protein, humanSTAT5 Transcription FactorTumor Suppressor Proteinsgene transcriptioninsulin-like growth factor-Isignal transducer and activator of transcriptionsignal transduction

Identifiers

PMID25205818
PMCPMC4216947
OpenAlexW1991275971

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.