Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

SNPs within the GH-signaling pathway are associated with the early IGF1 response to GH replacement therapy in GHD adults.

European journal of endocrinology - 1 Jan 2014

Glad Camilla A M, Barbosa Edna J L, Filipsson Nyström Helena, Carlsson Lena M S, Nilsson Staffan, Nilsson Anna G, Svensson Per-Arne, Johannsson Gudmundur

Abstract excerpt

OBJECTIVE: GH-deficient (GHD) adults have reduced serum concentrations of IGF1. GH replacement therapy increases serum IGF1 concentrations, but the interindividual variation in treatment response is large and likely influenced by genetic factors. This study was designed to test the hypothesis that single-nucleotide polymorphisms (SNPs) in genes within the GH signaling pathway influence the serum IGF1 response to...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Class I Phosphatidylinositol 3-Kinases
Share to Drug Monitoring

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hormone Replacement Therapy

Share to Human Growth Hormone

Share to Insulin-Like Growth Factor I

Share to Phosphatidylinositol 3-Kinases

Share to Receptors, Somatotropin

Share to Sweden

Source

Identifiers

PMID: 24114431
DOI: 10.1530/EJE-13-0685

Genes

IGF1
GHR
JAK2
SOCS2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SNPs within the GH-signaling pathway are associated with the early IGF1 response to GH replacement therapy in GHD adults.PMID 24114431Read ↗

The Exon 3-Deleted Growth Hormone Receptor (d3GHR) Polymorphism - a Favorable Backdoor Mechanism for the GHR FunctionSemantic proximity Read ↗

Genetic predictors of long-term response to growth hormone (GH) therapy in children with GH deficiency and Turner syndrome: the influence of a SOCS2 polymorphism.Semantic proximity Read ↗

A pharmacogenomic approach to the treatment of children with GH deficiency or Turner syndrome.Semantic proximity Read ↗

Genotypes associated with lipid metabolism contribute to differences in serum lipid profile of GH-deficient adults before and after GH replacement therapy.Semantic proximity Read ↗

Growth hormone pharmacogenetics: the interactive effect of a microsatellite in the IGF1 promoter region with the GHR-exon 3 and -202 A/C IGFBP3 variants on treatment outcomes of children with severe GH deficiency.Semantic proximity Read ↗

The signal transducer and activator of transcription 5B gene polymorphism contributes to the cholesterol metabolism in Japanese children with growth hormone deficiency.Semantic proximity Read ↗

Genetic determinants of growth hormone and GH-related phenotypes.Semantic proximity Read ↗

Pharmacogenomics of insulin-like growth factor-I generation during GH treatment in children with GH deficiency or Turner syndrome.Semantic proximity Read ↗

Abnormal GH Receptor Signaling in Children with Idiopathic Short StatureSemantic proximity Read ↗

The GH receptor exon 3 deletion is a marker of male-specific exceptional longevity associated with increased GH sensitivity and taller stature.Semantic proximity Read ↗

Molecular genetics of human growth hormone, insulin-like growth factors and their pathways in common disease.Semantic proximity Read ↗

The interactive effect of GHR-exon 3 and -202 A/C IGFBP3 polymorphisms on rhGH responsiveness and treatment outcomes in patients with Turner syndrome.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.