G3BP2 (G3BP Stress Granule Assembly Factor 2)

This cross-kingdom RNA delivery reprogrammed neuronal stress responses, reduced infarct volume, preserved neuronal morphology, and restored electrophysiological function. Collectively, our findings establish a scalable platform for plant-based nanotherapeutics and highlight the translational potential of NotoEV in treating ischemic stroke.

Clinically, analysis of a small set of CRC specimens suggests elevated YBX1 lactylation, consistent with its potential pathological relevance. Together, these results uncover a lactylation-dependent mechanism that governs m5C RNA recognition and contributes to YBX1's oncogenic activity.

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.

In adjuvant-induced arthritis (AA) rat models, intra-articular injection of compound C108 (4 and 8 μM) significantly alleviated arthritis symptoms, reduced synovial hyperplasia, downregulated G3BP2, N-cadherin, IL-1β, and MMP3 expression, while promoting p53 expression in FLSs of AA rats. Our findings demonstrate that G3BP2 promotes abnormal activation of RA-FLSs by suppressing p53 signaling, suggesting G3BP2 as a promising therapeutic target for RA treatment.

Moreover, knockout of Eps8l2 impairs CRC tumorigenesis in the AOM/DSS induced mouse model. In summary, we revealed a novel EPS8L2-YBX1-G3BP2 regulatory axis involved in CRC progression, which provides a new theoretical basis for tumor therapy.

Further, other insulin secretagogues such as exendin-4 and palmitate, but not high KCl, prompts the dissolution of G3BP1+/2+ condensates. G3BP1+/2+/Ins mRNA+ condensates are also found in primary mouse and human β-cells. Hence, G3BP1+/2+ condensates represent a conserved glycolysis/aldolase-regulated compartment for the physiological storage and protection of insulin mRNA in resting β-cells.

Furthermore, animal experiments confirm that administration of the in situ-formed droplets with sorafenib significantly inhibits tumor growth in murine models bearing tumors, accompanied by an excellent biosafety profile. The findings in this study elucidate an innovative approach for in situ formulation of coacervate droplets within tumor cells and a new material for targeting membraneless organelles, thus providing a promising new strategy for disease organelle-targeted therapy in the future.

Besides, ROBO1-mediated eIF3A degradation interrupted P53 translation process which in turn provoked downstream mTOR signaling and increased DNA repair associated genes expressions, resulting in radio-resistance enhancement in cancer cells. In conclusion, our findings revealed a novel role of eIF3A in modulating P53/mTOR signaling activity and provided a drug candidate (ROBO1) for overcoming radio-resistance in esophageal cancer.

Furthermore, network module analysis indicated transcription factors for oestrogen-related receptors to have a potential role during development of TGCT. The overlap between mRNA network hub genes and TGCT susceptibility genes indicates a common role in TGCT development.

Furthermore, DKC1 could bind to hENT mRNA and inhibited its expression, which enhanced gemcitabine resistance of PDAC. Therefore, we propose a novel mechanism wherein G3BP2 facilitates PDAC's resistance to chemotherapy by modulating PDIA3-DKC1-hENT in a SGs-dependent way, suggesting G3BP2 SGs a protentional therapeutic target for the treatment in PDAC.

Prognostic gene signature was predictive of DMFS for BCs with small tumor sizes. The protein-protein interaction network of PIK3R1, IL1R1, MMP11, GOLM1, and VAV3 connected by EGFR merits further experiments for elucidating the underlying mechanisms.

As demonstrated in our case cohort, 100% of cases diagnosed as high-grade follicular-derived thyroid carcinoma had a mutation or fusion that is associated with worse prognosis, has a germline syndrome association requiring further work up, or an actionable mutation. This high yield seen in this cohort for molecular testing in patients with high-grade follicular-derived thyroid carcinoma suggests more routine molecular testing in this population would be a beneficial clinical practice.