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@article{1834774,
author = {Margiotta, Azzurra},
article_location = {Basel},
article_number = {12},
doi = {http://dx.doi.org/10.3390/ijms22126342},
keywords = {RTKs; FGFRs; termination of signaling; degradation; ubiquitination; PTPs; kinases},
language = {eng},
issn = {1422-0067},
journal = {International Journal of Molecular Sciences},
title = {All Good Things Must End: Termination of Receptor Tyrosine Kinase Signal},
url = {https://www.mdpi.com/1422-0067/22/12/6342},
volume = {22},
year = {2021}
}
TY - JOUR
ID - 1834774
AU - Margiotta, Azzurra
PY - 2021
TI - All Good Things Must End: Termination of Receptor Tyrosine Kinase Signal
JF - International Journal of Molecular Sciences
VL - 22
IS - 12
SP - 1-14
EP - 1-14
PB - MDPI
SN - 14220067
KW - RTKs
KW - FGFRs
KW - termination of signaling
KW - degradation
KW - ubiquitination
KW - PTPs
KW - kinases
UR - https://www.mdpi.com/1422-0067/22/12/6342
N2 - Receptor tyrosine kinases (RTKs) are membrane receptors that regulate many fundamental cellular processes. A tight regulation of RTK signaling is fundamental for development and survival, and an altered signaling by RTKs can cause cancer. RTKs are localized at the plasma membrane (PM) and the major regulatory mechanism of signaling of RTKs is their endocytosis and degradation. In fact, RTKs at the cell surface bind ligands with their extracellular domain, become active, and are rapidly internalized where the temporal extent of signaling, attenuation, and downregulation are modulated. However, other mechanisms of signal attenuation and termination are known. Indeed, inhibition of RTKs' activity may occur through the modulation of the phosphorylation state of RTKs and the interaction with specific proteins, whereas antagonist ligands can inhibit the biological responses mediated by the receptor. Another mechanism concerns the expression of endogenous inactive receptor variants that are deficient in RTK activity and take part to inactive heterodimers or hetero-oligomers. The downregulation of RTK signals is fundamental for several cellular functions and the homeostasis of the cell. Here, we will review the mechanisms of signal attenuation and termination of RTKs, focusing on FGFRs.
ER -
MARGIOTTA, Azzurra. All Good Things Must End: Termination of Receptor Tyrosine Kinase Signal. \textit{International Journal of Molecular Sciences}. Basel: MDPI, 2021, roč.~22, č.~12, s.~1-14. ISSN~1422-0067. Dostupné z: https://dx.doi.org/10.3390/ijms22126342.
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