G3BP1 (G3BP Stress Granule Assembly Factor 1)

Understanding the interplay between retroviruses and stress granule biology provides insight into host-virus coevolution and identifies potential therapeutic targets to restore antiviral stress responses. Targeting SG-associated pathways may represent a novel strategy to limit retroviral replication and virus-induced pathogenesis.

By integrating these findings, we aim to provide an up-to-date framework that not only highlights the novelty of recent G3BP-directed modulators but also addresses prior reviewer concerns regarding overlap with existing literature-emphasizing how our synthesis uniquely compiles both SG inhibitors and "agonists" in one analysis. Ultimately, leveraging the G3BP1/2-SG axis may enable multi-pathway reprogramming of stress responses for therapeutic benefit.

WFDC21P knockdown in TNBC cells markedly dampens RIG-I activation and reduces the expression of IFN-stimulated genes, including MHC-I and PD-L1. In syngeneic tumor models, WFDC21P expression not only suppresses tumor growth by augmenting the infiltration and cytotoxic function of CD8+ T cells but also improves the response to immune checkpoint blockade, thus providing a compelling combination immunotherapy strategy for treating triple-negative breast cancer.

In our analysis, G3BP2 was not associated with survival benefit. However, clear associations were observed between altered expression of this gene and a number of important pathways linked to cancer pathogenesis, and further studies are warranted to assess this gene (and/or) stress granules in cancer.

In vivo, disruption of the NUP93/SOX2/G3BP1 axis suppressed tumor growth and synergized with gemcitabine. Our findings unveil the novel NUP93-SOX2-G3BP1 signaling axis as a critical driver of gemcitabine resistance in PDAC, presenting a promising therapeutic target for overcoming chemoresistance.

Label‑free mass spectrometry identified G3BP1, SLIRP and IGFBP5 as AR interactors linked to stress response, metabolic adaptation and ERα repression. The findings of this study highlight the prognostic potential of cytoplasmic AR immunoreactivity in specific breast cancer subtypes and uncover novel cytoplasmic AR protein interactions that may mediate metabolic adaptations during the development of endocrine-resistance.

Integration with high-content screening enabled quantitative, image-based analysis of cellular stress phenotypes, greatly enhancing throughput and mechanistic insight, thereby provided next-generation New Approach Methodologies for lung toxicity assessment. Together, this hiPSC-derived lung organoid SG reporter platform links early molecular stress adaptation to tissue-level responses, offering a predictive and mechanistically informative framework for human-relevant lung toxicity evaluation.

This modeling places the PRRC2C α helix in a previously unassigned region of a published cryo-EM density map, validating the protein interaction and the mechanistic role of PRRC2C in translation control. Together, these findings establish PRRC2 proteins as components of the translation initiation machinery that regulate translation through their interactions with the eIF3 complex and other components of the 48S PIC factors, providing a direct mechanistic link between stress granule proteins and translational control.

Collectively, our findings demonstrate that hypoxia-induced PABP1/eIF4B LLPS specifically upregulates ChaC2 expression, enabling metastatic cancer cells to evade ferroptosis triggered by their own metastatic demands and ultimately facilitating tumor dissemination. This study uncovers a critical adaptive regulatory mechanism employed by metastatic GC cells to cope with stress challenges during PM, thereby offering novel therapeutic targets and strategic insights for intervention.

Additionally, G3BP2 is closely associated with various non-tumor diseases, including viral infections, as well as cardiovascular and cerebrovascular diseases. This review elucidates the role of G3BP2 in the development and progression of various diseases, identifying biomarkers and therapeutic targets for clinical diagnosis and treatment based on G3BP2.

Its upregulation promotes tumor progression by activating the PI3K/AKT/mTOR signaling pathway and modulating the tumor immune microenvironment. These findings provide a theoretical foundation for targeting G3BP1 in BRCA diagnosis and immunotherapy.

YsF-LSG peptide mixtures reverse SFR of HCC through G3BP2-recruited, SGs-targeting and apoptosis-restored mechanisms. This provides a new strategy for developing enzyme-induced LLPS peptide coacervates with drug resistance-reversal capacity.