ArticlePloS one2012
Insulin-like growth factor-I E-peptide activity is dependent on the IGF-I receptor.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Chloroplast transformation for bioencapsulation and oral delivery using the immunoglobulin G fragment crystallizable (Fc) domain.Scientific reports · 2023Article
- Lower muscle protein synthesis in humans with obesity concurrent with lower expression of muscle IGF1 splice variants.Obesity (Silver Spring, Md.) · 2023Article
- Variation of insulin-related peptides accompanying the differentiation ofEcology and evolution · 2023Article
- The role of mechano growth factor in chondrocytes and cartilage defects: a concise review.Acta biochimica et biophysica Sinica · 2023Review
- Mechano-growth factor E-domain modulates cardiac contractile function through 14-3-3 protein interactomes.Frontiers in physiology · 2022Article
- Molecular cloning, expression, and functional features of IGF1 splice variants in sheep.Endocrine connections · 2021Article
- Role of Alternatively Spliced Messenger RNA (mRNA) Isoforms of the Insulin-Like Growth Factor 1 (IGF1) in Selected Human Tumors.International journal of molecular sciences · 2020Review
- CRISPR-Cas9-induced IGF1 gene activation as a tool for enhancing muscle differentiation via multiple isoform expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The structure-function relationships of insulin-like growth factor 1 Ec in C2C12 cells.Cell adhesion & migration · 2018Article
- Overexpression of Mechano-Growth Factor Modulates Inflammatory Cytokine Expression and Macrophage Resolution in Skeletal Muscle Injury.Frontiers in physiology · 2018Article
- Article
- Prevalence of diabetes and obesity in association with prematurity and growth restriction.Diabetes, metabolic syndrome and obesity : targets and therapy · 2017Review
- Article
- Increased IGF-IEc expression and mechano-growth factor production in intestinal muscle of fibrostenotic Crohn's disease and smooth muscle hypertrophy.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Review
- Changes in Communication between Muscle Stem Cells and their Environment with Aging.Journal of neuromuscular diseases · 2015Article
- Localized delivery of mechano-growth factor E-domain peptide via polymeric microstructures improves cardiac function following myocardial infarction.Biomaterials · 2015Article
- Oncogenic Role of the Ec Peptide of the IGF-1Ec Isoform in Prostate Cancer.Molecular medicine (Cambridge, Mass.) · 2015Article
- Optimizing IGF-I for skeletal muscle therapeutics.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2014Review
- IGF expression in HPV-related and HPV-unrelated human cancer cells.Oncology reports · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Insulin-like growth factor-I (IGF-I) is an essential growth factor that regulates the processes necessary for cell proliferation, differentiation, and survival. The Igf1 gene encodes mature IGF-I and a carboxy-terminal extension called the E-peptide. In rodents, alternative splicing and post-translational processing produce two E-peptides (EA and EB). EB has been studied extensively and has been reported to promote cell proliferation and migration independently of IGF-I and its receptor (IGF-IR), but the mechanism by which EB causes these actions has not been identified. Further, the properties of EA have not been evaluated. Therefore, the goals of this study were to determine if EA and EB possessed similar activity and if these actions were IGF-IR independent. We utilized synthetic peptides for EA, EB, and a scrambled control to examine cellular responses. Both E-peptides increased MAPK signaling, which was blocked by pharmacologic IGF-IR inhibition. Although the E-peptides did not directly induce IGF-IR phosphorylation, the presence of either E-peptide increased IGF-IR activation by IGF-I, and this was achieved through enhanced cell surface bioavailability of the receptor. To determine if E-peptide biological actions required the IGF-IR, we took advantage of the murine C2C12 cell line as a platform to examine the key steps of skeletal muscle proliferation, migration and differentiation. EB increased myoblast proliferation and migration while EA delayed differentiation. The proliferation and migration effects were inhibited by MAPK or IGF-IR signaling blockade. Thus, in contrast to previous studies, we find that E-peptide signaling, mitogenic, and motogenic effects are dependent upon IGF-IR. We propose that the E-peptides have little independent activity, but instead affect growth via modulating IGF-I signaling, thereby increasing the complexity of IGF-I biological activity.
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Registered trials
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.