scholarly journals Dexamethasone enhances insulin-like growth factor-I effects on skeletal muscle cell proliferation. Role of specific intracellular signaling pathways.

1995 ◽  
Vol 96 (3) ◽  
pp. 1473-1483 ◽  
Author(s):  
F Giorgino ◽  
R J Smith
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Muscle Cell ◽  
Intracellular Signaling ◽  
Skeletal Muscle Cell ◽  
Factor I ◽  
Intracellular Signaling Pathways

scholarly journals The IGF-1 Signaling Pathway in Viral Infections

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1488
Author(s):  
Agata Józefiak ◽  
Magdalena Larska ◽  
Małgorzata Pomorska-Mól ◽  
Jakub J. Ruszkowski
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Intracellular Signaling ◽  
Viral Infections ◽  
Mapk Pathway ◽  
Mitogen Activated Protein Kinase ◽  
Insulin Like Growth Factor ◽  
Intracellular Signaling Pathways

Insulin-like growth factor-1 (IGF-1) and the IGF-1 receptor (IGF-1R) belong to the insulin-like growth factor family, and IGF-1 activates intracellular signaling pathways by binding specifically to IGF-1R. The interaction between IGF-1 and IGF-1R transmits a signal through a number of intracellular substrates, including the insulin receptor substrate (IRS) and the Src homology collagen (Shc) proteins, which activate two major intracellular signaling pathways: the phosphatidylinositol 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) pathways, specifically the extracellular signal-regulated kinase (ERK) pathways. The PI3K/AKT kinase pathway regulates a variety of cellular processes, including cell proliferation and apoptosis. IGF1/IGF-1R signaling also promotes cell differentiation and proliferation via the Ras/MAPK pathway. Moreover, upon IGF-1R activation of the IRS and Shc adaptor proteins, Shc stimulates Raf through the GTPase Ras to activate the MAPKs ERK1 and ERK2, phosphorylate and several other proteins, and to stimulate cell proliferation. The IGF-1 signaling pathway is required for certain viral effects in oncogenic progression and may be induced as an effect of viral infection. The mechanisms of IGF signaling in animal viral infections need to be clarified, mainly because they are involved in multifactorial signaling pathways. The aim of this review is to summarize the current data obtained from virological studies and to increase our understanding of the complex role of the IGF-1 signaling axis in animal virus infections.

Invited Review: Autocrine/paracrine IGF-I and skeletal muscle adaptation

2002 ◽  
Vol 93 (3) ◽  
pp. 1159-1167 ◽  
Author(s):  
Gregory R. Adams
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Muscle Hypertrophy ◽  
Muscle Adaptation ◽  
Factor I ◽  
Important Mediator ◽  
Signaling Mechanisms ◽  
Igf I

This brief review presents the basic premises suggesting that insulin-like growth factor I (IGF-I), functioning in an autocrine/paracrine mode, is an important mediator of skeletal muscle adaptation. Key intracellular signaling mechanisms associated with ligation of the primary IGF-I receptor are highlighted to illustrate the mechanisms by which IGF-I may promote muscle hypertrophy. In addition, a number of recent findings are presented that highlight the potential for interactions between IGF-I-related signaling pathways and intracellular signaling mechanisms activated by cytokines or hormonal systems.

scholarly journals Nanodelivery Systems Targeting Epidermal Growth Factor Receptors for Glioma Management

Pharmaceutics ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 1198
Author(s):  
Sathishbabu Paranthaman ◽  
Meghana Goravinahalli Shivananjegowda ◽  
Manohar Mahadev ◽  
Afrasim Moin ◽  
Shivakumar Hagalavadi Nanjappa ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Protein Kinase ◽  
Cell Surface ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Future Research ◽  
Extensive Literature ◽  
Egfr Tkis

A paradigm shift in treating the most aggressive and malignant form of glioma is continuously evolving; however, these strategies do not provide a better life and survival index. Currently, neurosurgical debulking, radiotherapy, and chemotherapy are the treatment options available for glioma, but these are non-specific in action. Patients invariably develop resistance to these therapies, leading to recurrence and death. Receptor Tyrosine Kinases (RTKs) are among the most common cell surface proteins in glioma and play a significant role in malignant progression; thus, these are currently being explored as therapeutic targets. RTKs belong to the family of cell surface receptors that are activated by ligands which in turn activates two major downstream signaling pathways via Rapidly Accelerating Sarcoma/mitogen activated protein kinase/extracellular-signal-regulated kinase (Ras/MAPK/ERK) and phosphatidylinositol 3-kinase/a serine/threonine protein kinase/mammalian target of rapamycin (PI3K/AKT/mTOR). These pathways are critically involved in regulating cell proliferation, invasion, metabolism, autophagy, and apoptosis. Dysregulation in these pathways results in uncontrolled glioma cell proliferation, invasion, angiogenesis, and cancer progression. Thus, RTK pathways are considered a potential target in glioma management. This review summarizes the possible risk factors involved in the growth of glioblastoma (GBM). The role of RTKs inhibitors (TKIs) and the intracellular signaling pathways involved, small molecules under clinical trials, and the updates were discussed. We have also compiled information on the outcomes from the various endothelial growth factor receptor (EGFR)–TKIs-based nanoformulations from the preclinical and clinical points of view. Aided by an extensive literature search, we propose the challenges and potential opportunities for future research on EGFR–TKIs-based nanodelivery systems.

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