J 2021

All Good Things Must End: Termination of Receptor Tyrosine Kinase Signal

MARGIOTTA, Azzurra

Basic information

Original name

All Good Things Must End: Termination of Receptor Tyrosine Kinase Signal

Authors

MARGIOTTA, Azzurra (380 Italy, guarantor, belonging to the institution)

Edition

International Journal of Molecular Sciences, Basel, MDPI, 2021, 1422-0067

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

10608 Biochemistry and molecular biology

Country of publisher

Switzerland

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 6.208

RIV identification code

RIV/00216224:14110/21:00124195

Organization unit

Faculty of Medicine

DOI

UT WoS

000665932000001

Keywords in English

RTKs; FGFRs; termination of signaling; degradation; ubiquitination; PTPs; kinases

Tags

Tags

International impact, Reviewed
Změněno: 5/4/2022 13:41, Mgr. Tereza Miškechová

Abstract

V originále

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.