PACAP type I receptor transactivation is essential for IGF‐1 receptor signalling and antiapoptotic activity in neurons [PDF]
Insulin-like growth factor-1 (IGF-1) and pituitary adenylyl cyclase activating polypeptide (PACAP) are both potent neurotrophic and antiapoptotic factors, which exert their effects via phosphorylation cascades initiated by tyrosine kinase and G-protein-coupled receptors, respectively. Here, we have adapted a recently described phosphoproteomic approach
Nicolas, Delcourt +6 more
core +5 more sources
IGF-I and insulin activate mitogen-activated protein kinase via the type 1 IGF receptor in mouse embryonic stem cells [PDF]
Abstract Although IGF-I and insulin are important modulators of preimplantation embryonic physiology, the signalling pathways activated during development remain to be elucidated. As a model of preimplantation embryos, pluripotent mouse embryonic stem cells were used to investigate which receptor mediated actions of physiological ...
Nguyen, T. T. +3 more
openaire +6 more sources
IGF2 knockout reduces but does not abolish osteosarcoma growth in vitro and in vivo. [PDF]
To test whether endogenous IGF2 promotes osteosarcoma growth, IGF2 was knocked out in Saos2 cells via CRISPR‐Cas9. KO cells showed reduced proliferation in vitro, and knockout xenografts in mice reached only ~25% of wild‐type tumor volume. Insulin‐like growth factor 2 (IGF2) is implicated in osteosarcoma, but direct functional evidence of its role is ...
Yao S, Archetti M.
europepmc +2 more sources
Loss of IGF-1R impairs DNA-PKcs recruitment to chromatin leading to defective end-joining. [PDF]
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Ellis MO +3 more
europepmc +2 more sources
Regulation of human fibroblast insulin-like growth factor (IGF)-binding proteins by IGF-1 and cytokines, mechanisms of action and effects upon IGF bioactivity [PDF]
PhDThe insulin-like growth factors, IGF-I and IGF-II, are ubiquitous polypeptide molecules that have mitogenic and metabolic actions in a wide variety of cell types, and consequently play a major role in mammalian growth and development.
Yateman, Martin Edward
core +4 more sources
The GH-IGF-I axis and breast cancer [PDF]
MD (Res)Breast cancer remains one of the most common causes of death amongst women today. Worldwide approximately 1.3 million women are diagnosed as having breast cancer every year.
Laban, Christiana
core +4 more sources
Cumulative mutagenesis of the basic residues in the 201-218 region of insulin-like growth factor (IGF)-binding protein-5 results in progressive loss of both IGF-I binding and inhibition of IGF-I biological action [PDF]
We have reported previously that mutation of two conserved nonbasic amino acids (G203 and Q209) within the highly basic 201–218 region in the C-terminal domain of IGF-binding protein-5 (IGFBP-5) decreases binding to IGFs.
Clegg, R.A. +9 more
core +4 more sources
IGF Type 1 Receptor: A Cell Cycle Progression Factor That Regulates Aging [PDF]
International ...
Dupont, Joëlle, Holzenberger, M.
openaire +3 more sources
The IGF/Insulin-IGFBP Axis in Corneal Development, Wound Healing, and Disease
The insulin-like growth factor (IGF) family plays key roles in growth and development. In the cornea, IGF family members have been implicated in proliferation, differentiation, and migration, critical events that maintain a smooth refracting surface that
Whitney L. Stuard +2 more
doaj +1 more source
Insulin-Like Growth Factor II (IGF-II) Is More Potent Than IGF-I in Stimulating Cortisol Secretion from Cultured Bovine Adrenocortical Cells: Interaction with the IGF-I Receptor and IGF-Binding Proteins [PDF]
Although the stimulating effect of insulin-like growth factor I (IGF-I) on adrenal steroidogenesis has been well established, the role of IGF-II in the adult adrenal gland remains unknown.
Weber, Matthias M. +4 more
core +2 more sources

