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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, vol.~22, No~12, p.~1-14. ISSN~1422-0067. Available from: https://dx.doi.org/10.3390/ijms22126342.
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