Identification of an inhibitory domain in GTPase-activating protein p190RhoGAP responsible for masking its functional GAP domain

Heraud, Capucine; Pinault, Mathilde; Neaud, Véronique; Saltel, Frédéric; Lagrée, Valérie; Moreau, Violaine

doi:10.1016/j.jbc.2022.102792

Cited by 2 publications

(1 citation statement)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our study, we suggest that eIF3h and eIF3d drive respectively canonical and non-canonical translation while eIF3e, acts at the interconnection of both modes of translation in accordance to its own role in the dynamic of the eIF3 complex, formation 12 , explaining the huge effects of eIF3e depletion in protein synthesis in NIH-3T3 Src cells. A another study confirmed the interest to study eIF3 complex in invadosomes since 11 of the 13 eIF3 subunits were found to interact with p190RhoGAP 40 a key driver of invadosome formation 41 .…”

Section: Discussionmentioning

confidence: 82%

Src promotes tumor cell invasion by hijacking the translation machinery

Bonnard,

Chatefau,

Dourthe

et al. 2024

Preprint

View full text Add to dashboard Cite

The Src oncogene controls cancer cell invasiveness by promoting invadosome formation and extracellular matrix degradation (ECM). Invadosomes are enriched in the eukaryotic translation initiation factor 3 (eIF3) complex associated with a local mRNA translation activity mandatory for their maintenance. Here, we show that Src regulates mRNA translation by controlling the expression of eIF3 subunits. Among them, eIF3h/e/d are essential for invadosome formation and ECM degradation. We demonstrate that Src controls the canonical mTOR/eIF4E and the non-canonical eIF3d cap-dependent translation initiation pathways. We show that both pathways are necessary for invadosome formation and their ECM degradation function. Finally, we highlighted a correlation betweenSrcandeIF3h/e/doverexpression, which is associated with poor prognosis in hepatocellular carcinoma (HCC) patients and controls the ECM degradation and invasive properties of HCC cells. These findings identify Src as a major regulator of translation initiation pathways, which leads to invadosome formation, ECM degradation and tumor cell invasion.Abstract FigureGraphical abstract

show abstract

Section: Discussionmentioning

confidence: 82%

Src promotes tumor cell invasion by hijacking the translation machinery

Bonnard,

Chatefau,

Dourthe

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

Roles of G proteins and their GTPase-activating proteins in platelets

O'Donoghue,

Smolenski

2024

Bioscience Reports

View full text Add to dashboard Cite

Platelets are small anucleate blood cells supporting vascular function. They circulate in a quiescent state monitoring the vasculature for injuries. Platelets adhere to injury sites and can be rapidly activated to secrete granules and to form platelet/platelet aggregates. These responses are controlled by signalling networks that include G proteins and their regulatory guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Recent proteomics studies have revealed the complete spectrum of G proteins, GEFs, and GAPs present in platelets. Some of these proteins are specific for platelets and very few have been characterised in detail. GEFs and GAPs play a major role in setting local levels of active GTP-bound G proteins in response to activating and inhibitory signals encountered by platelets. Thus, GEFs and GAPs are highly regulated themselves and appear to integrate G protein regulation with other cellular processes. This review focuses on GAPs of small G proteins of the Arf, Rab, Ras, and Rho families, as well as of heterotrimeric G proteins found in platelets.

show abstract

Identification of an inhibitory domain in GTPase-activating protein p190RhoGAP responsible for masking its functional GAP domain

Cited by 2 publications

References 30 publications

Src promotes tumor cell invasion by hijacking the translation machinery

Src promotes tumor cell invasion by hijacking the translation machinery

Roles of G proteins and their GTPase-activating proteins in platelets

Contact Info

Product

Resources

About