Evidence map›Paper›PMID 17308965›Full record

ReviewReviews in endocrine & metabolic disorders2006

Recent advances in growth hormone signaling.

Nathan J Lanning, Christin Carter-Su

Abstract readReview
PubMed Publisher
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 230 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Centrosomal JAK2 Tyrosine Kinase Regulates Primary Cilia Length, Cell Proliferation, and Cilia Orientation During Cell Migration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. GHRH in diabetes and metabolism.Reviews in endocrine & metabolic disorders · 2025
    Review
  10. Central and peripheral regulation of the GH/IGF-1 axis: GHRH and beyond.Reviews in endocrine & metabolic disorders · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Ghrelin regulating liver activity and its potential effects on liver fibrosis andFrontiers in cellular and infection microbiology · 2023
    Review
  17. Activated phosphoinositide 3-kinase δ syndrome associated with nephromegaly, growth hormone deficiency, bronchiectasis: a case report.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022
    Article
  18. Article
  19. Renal effects of growth hormone in health and in kidney disease.Pediatric nephrology (Berlin, Germany) · 2021
    Article
  20. Review

37 more citing papers are in PubMed but not listed here.

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.

Nathan J LanningCellular and Molecular Biology Graduate Program, University of Michigan Medical School, 1301 Catherine Street, Ann Arbor, MI 48109-0622, USA. lanningn@umich.edu
Christin Carter-Su
University of Michigan–Ann Arbor · US

Funding

CELLULAR AND MOLECULAR BIOLOGY AT MICHIGANT32GM007315 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PUTHENVEEDU, MANOJKUMAR A · 1985 to 2021
$12.8M
Growth Hormone Regulation of SH2B1R01DK054222 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARTER-SU, CHRISTIN · 1999 to 2020
$7.7M
TRAINING PROGRAM IN ORGANOGENESIST32HD007505 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PASCA DI MAGLIANO, MARINA, SPENCE, JASON · 1997 to 2021
$6.9M
Growth Hormone Receptors and ActionsR37DK034171 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARTER-SU, CHRISTIN · 2001 to 2010
$3.8M
GROWTH HORMONE RECEPTORS AND ACTIONSR01DK034171 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARTER-SU, CHRISTIN · 1986 to 2000
$256k
NICHD NIH HHS T-32-HD007505NIDDK NIH HHS R01 DK054222NIDDK NIH HHS R01-DK34171NIDDK NIH HHS R37 DK034171NIGMS NIH HHS T32 GM007315
6 · The paper itself

Abstract

Growth hormone (GH) is a major regulatory factor for overall body growth as evidenced by the height extremes in people with abnormal circulating GH levels or GH receptor (GHR) disruptions. GH also affects metabolism, cardiac and immune function, mental agility and aging. Currently, GH is being used therapeutically for a variety of clinical conditions including promotion of growth in short statured children, treatment of adults with GH deficiency and HIV-associated wasting. To help reveal previous unrecognized functions of GH, better understand the known functions of GH, and avoid adverse consequences that are often associated with exogenous GH administration, careful delineation of the molecular mechanisms whereby GH induces its diverse effects is needed. GH is a peptide hormone that is secreted into the circulation by the anterior pituitary and acts upon various target tissues expressing GHR. GH binding of GHR activates the tyrosine kinase Janus kinase 2 (JAK2), thus initiating a multitude of signaling cascades that result in a variety of biological responses including cellular proliferation, differentiation and migration, prevention of apoptosis, cytoskeletal reorganization and regulation of metabolic pathways. A number of signaling proteins and pathways activated by GH have been identified, including JAKs, signal transducers and activators of transcription (Stats), the mitogen activated protein kinase (MAPK) pathway, and the phosphatidylinositol 3'-kinase (PI3K) pathway. Although these signal transduction pathways have been well characterized, the manner by which GH activates these pathways, the downstream signals induced by these pathways, and the cross-talk with other pathways are not completely understood. Recent findings have added vital information to our understanding of these downstream signals induced by GH and mechanisms that terminate GH signaling, and identified new GH signaling proteins and pathways. This review will highlight some of these findings, many of which are unexpected and some of which challenge previously held beliefs about the mechanisms of GH signaling.

Indexed as

AnimalsGrowth HormoneHumansMitogen-Activated Protein KinasesModels, BiologicalProtein Tyrosine PhosphatasesSignal TransductionSTAT Transcription FactorsTYK2 KinaseGrowth HormoneMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesSTAT Transcription FactorsTYK2 Kinase

Identifiers

PMID17308965
OpenAlexW1990076171

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.