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

J 2021

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

MARGIOTTA, Azzurra

Základní údaje

Originální název

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

Autoři

MARGIOTTA, Azzurra (380 Itálie, garant, domácí)

Vydání

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

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10608 Biochemistry and molecular biology

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 6.208

Kód RIV

RIV/00216224:14110/21:00124195

Organizační jednotka

Lékařská fakulta

DOI

http://dx.doi.org/10.3390/ijms22126342

UT WoS

000665932000001

Klíčová slova anglicky

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

Štítky

14110513, rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 5. 4. 2022 13:41, Mgr. Tereza Miškechová

Anotace

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.

Citovat

MARGIOTTA, Azzurra. All Good Things Must End: Termination of Receptor Tyrosine Kinase Signal. 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.

@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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