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Cell cycle control by the insulin-like growth factor signal: at the crossroad between cell growth and mitotic regulation
Fujita-Yamaguchi, Yoko Giordano, Antonio
Fujita-Yamaguchi, Yoko
Giordano, Antonio
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Genre
Journal article
Date
2022-08-25
Advisor
Committee member
Group
Department
Biology
Subject
GF
Growth factor
Trophic (effect)
Property of a GF to increase growth (hypertrophy) and number (hyperplasia) of a target cell or tissue
GH
Growth hormone
RTK
Receptor tyrosine kinase
IGF-I/II: insulin like growth factor peptides
igf1/2
Insulin like growth factor genes
igf1r
IGF-Type I receptor gene
IGF1R
Insulin-like growth factor receptortype I (protein)
Insr
Insulin receptor gene
IR (also InsR)
Insulin receptor protein
IR-A
IR isoform A (exon 11-)
HybR
IGF1R/IR hybrid receptor
HybR-A
IGF1R/IR-A
igf2r/m6pr/SpI2-6
(scavenger protein for IGF2 & mannose-6-phosphate)
Trans-membrane high affinity IGF2 scavenger protein
IRS
Insulin receptor substrate
mTOR
Mammalian target of rapamycin
mTORC
mTOR complex
Growth factor
Trophic (effect)
Property of a GF to increase growth (hypertrophy) and number (hyperplasia) of a target cell or tissue
GH
Growth hormone
RTK
Receptor tyrosine kinase
IGF-I/II: insulin like growth factor peptides
igf1/2
Insulin like growth factor genes
igf1r
IGF-Type I receptor gene
IGF1R
Insulin-like growth factor receptortype I (protein)
Insr
Insulin receptor gene
IR (also InsR)
Insulin receptor protein
IR-A
IR isoform A (exon 11-)
HybR
IGF1R/IR hybrid receptor
HybR-A
IGF1R/IR-A
igf2r/m6pr/SpI2-6
(scavenger protein for IGF2 & mannose-6-phosphate)
Trans-membrane high affinity IGF2 scavenger protein
IRS
Insulin receptor substrate
mTOR
Mammalian target of rapamycin
mTORC
mTOR complex
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Journal Issue
DOI
http://dx.doi.org/10.1080/15384101.2022.2108117
Abstract
In proliferating cells and tissues a number of checkpoints (G1/S and G2/M) preceding cell division (M-phase) require the signal provided by growth factors present in serum. IGFs (I and II) have been demonstrated to constitute key intrinsic components of the peptidic active fraction of mammalian serum. In vivo genetic ablation studies have shown that the cellular signal triggered by the IGFs through their cellular receptors represents a non-replaceable requirement for cell growth and cell cycle progression. Retroactive and current evaluation of published literature sheds light on the intracellular circuitry activated by these factors providing us with a better picture of the pleiotropic mechanistic actions by which IGFs regulate both cell size and mitogenesis under developmental growth as well as in malignant proliferation. The present work aims to summarize the cumulative knowledge learned from the IGF ligands/receptors and their intracellular signaling transducers towards control of cell size and cell-cycle with particular focus to their actionable circuits in human cancer. Furthermore, we bring novel perspectives on key functional discriminants of the IGF growth-mitogenic pathway allowing re-evaluation on some of its signal components based upon established evidences.
Description
Citation
Scalia, P., Williams, S. J., Fujita-Yamaguchi, Y., & Giordano, A. (2023). Cell cycle control by the insulin-like growth factor signal: at the crossroad between cell growth and mitotic regulation. Cell Cycle, 22(1), 1–37. https://doi.org/10.1080/15384101.2022.2108117
Citation to related work
Taylor and Francis Group
Has part
Cell Cycle, Vol. 22, Iss. 1
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