<unk>  is a primary mediator of the effects of growth hormone (GH). Growth hormone is made in the anterior pituitary gland, is released into the blood stream, and then stimulates the liver to produce<unk> .<unk>  then stimulates systemic body growth, and has growth-promoting effects on almost every cell in the body, especially skeletal muscle, cartilage, bone, liver, kidney, nerve, skin, hematopoietic, and lung cells. In addition to the<unk> -like effects,<unk>  can also regulate cellular DNA synthesis.<unk>  binds to at least two cell surface receptor tyrosine kinases: the<unk>  receptor <unk> R), and the<unk>  receptor. Its primary action is mediated by binding to its specific receptor,<unk> R, which is present on the surface of many cell types in many tissues. Binding to the<unk> R initiates intracellular signaling.<unk>  is one of the most potent natural activators of the AKT signaling pathway, a stimulator of cell growth and proliferation, and a potent inhibitor of programmed cell death . The<unk>  receptor seems to be the "physiologic" receptor because it binds<unk>  with significantly higher affinity than<unk>  receptor does.<unk>  activates the<unk>  receptor at approximately 0.1 times the potency of<unk> . Part of this signaling may be via<unk> R/Insulin Receptor heterodimers (the reason for the confusion is that binding studies show that<unk>  binds the<unk>  receptor<unk> 00-fold less well than<unk> , yet that does not correlate with the actual potency of<unk>  in vivo at inducing phosphorylation of the<unk>  receptor, and hypoglycemia).<unk>  binds and activates its own receptor,<unk> R, through the cell surface expression of Receptor Tyrosine Kinase's (RTK's) and further signal through multiple intracellular transduction cascades.<unk> R is the critical role-playing inducer in modulating the metabolic effects of<unk>  for cellular senescence and survival. At a localized target cell,<unk> R elicits the mediation of paracrine activity. After its activation the initiation of intracellular signaling occurs inducing a magnitude of signaling pathways. An important mechanistic pathway involved in mediating a cascade affect a key pathway regulated by phosphatidylinositol-3 kinase (PI3K) and its downstream partner, mTOR (mammalian Target of Rapamycin). Rapamycin binds with the enzyme FKBPP12 to inhibit the mTORC1 complex. mTORC2 remains unaffected and responds by up-regulating AKT, driving signals through the inhibited mTORC1. Phosphorylation of Eukaryotic translation initiation<unk>  4E (EIF4E) by mTOR suppresses the capacity of Eukaryotic translation initiation<unk>  4E-binding protein<unk>  (EIF4EBP1) to inhibit EIF4E and slow metabolism. A mutation in the signaling pathway PI3K-AKT-mTOR is a big<unk>  in the formation of tumors found predominantly on skin, internal organs, and secondary lymph nodes (Kaposi sarcoma).<unk> R allows the activation of these signaling pathways and subsequently regulates the cellular longevity and metabolic re-uptake of biogenic substances. A therapeutic approach targeting towards the reduction of such tumor collections could be induced by ganitumab. Ganitumab is a monoclonal antibody (mAb) directed antagonistically against<unk> R. Ganitumab binds to<unk> R, preventing binding of<unk>  and the subsequent triggering of the PI3K-mTOR signaling pathway; inhibition of this pro-survival pathway may result in the inhibition of tumor cell expansion and the induction of tumor cell apoptosis.<unk>  has been shown to bind and interact with all seven<unk>  binding proteins (IGFBPs): IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, IGFBP6, and IGFBP7. Some IGFBPs are inhibitory. For example, both IGFBP-2 and IGFBP-5 bind<unk>  at a higher affinity than it binds its receptor. Therefore, increases in serum levels of these two IGFBPs result in a decrease in<unk>  activity.
Insulin-like growth factor 1
Keratinocyte growth factor
Calcitonin gene-related peptide
Growth hormone
Bryostatin
Orexin
Neurotrophic factors
Hemopoietic growth factor