RAB11A (RAB11A, Member RAS Oncogene Family)

This trafficking governed key metastatic features of TNBC, including β1 integrin recycling and α3β1 integrin surface exposure. Inhibition of SH3BP5L or its GEF activity reduced cell spreading in zebrafish and lung metastasis in mouse models, revealing a previously unidentified driver of BC dissemination and a potential therapeutic vulnerability.

Critically, pharmacological or genetic inhibition of cathepsin B restored meiotic progression in CCDC41-deficient oocytes. Collectively, the findings establish that CCDC41 is essential for faithful meiotic completion, it regulates CDC20 activity through promoting cathepsin delivery to lysosomes, and ensures proper spindle migration via Rab11a-dependent F-actin anchoring.

TMEM199/CCDC115 also recruits transport protein particle (TRAPP) Ⅱ to the recycling endosomes and activates RAB11A, leading to enhanced IFNGR1/2 recycling and downstream PD-L1 upregulation. Collectively, these findings reveal that TMEM199 might be a promising therapeutic target for immunotherapy.

Among the identified small molecules, three candidates were further validated to interfere with both RAB11A activation and GLUT3 trafficking, highlighting their potential as metabolic regulators. Our NanoBRET-based biosensor provides a robust and scalable platform for high-throughput screening of PPI inhibitors, offering a promising strategy for developing novel therapeutics targeting PPIs.

Gemcitabine-based chemotherapy remains a cornerstone in pancreatic cancer treatment, yet its efficacy is hindered by poor bioavailability and adaptive resistance mechanisms, such as autophagy...In addition, RNA sequencing and flow cytometry analyses revealed that HA/ZIF-8@BPP/Gem stimulated the secretion of immune-related cytokines and activated immune response pathways, particularly T cell-mediated immunity. In conclusion, our study presents a safe and effective strategy of nano-enabled drug repurposing to improve chemotherapy outcomes by inducing amplified autophagy arrest and immune activation in pancreatic cancer.

Furthermore, overexpression of related Rab proteins with overlapping functions does not rescue the cytokinetic defects caused by Rab11 or Rab35 downregulation in cancer cells. Therefore, this study aims to deepen our understanding of how Rab11 and Rab35 orchestrate the molecular events that drive the progression from late anaphase through the completion of cytokinesis.

Urinary exosomal RAB11A shows promise as a non-invasive biomarker for SCLC diagnosis, treatment response monitoring, and early detection of relapse, potentially improving clinical management of SCLC patients. The findings provide insights into SCLC pathogenesis and offer a non-invasive approach for patient monitoring, which could improve clinical management strategies.

Further, PPI analysis was performed to predict the interactions between immune-related DEPs, which were mainly divided into proteins directly involved in immune regulation (such as HSP90B1, LAMP1, CALR, and RAB11A) and proteins indirectly involved in immune regulation by vesicle transport (such as TSG101, VAMP3, SNAP25, RAB14, and RAB2). These findings reveal that EVs play a central role in mediating innate immune regulation in C. farreri via cell communication under LPS stimulation, and are expected to provide important insights into disease-resistant breeding and aquaculture practices in shellfish.

Here, we adopt a magnetogenetic approach that allows direct manipulation of Rab25 positioning to show that localization to the cell periphery drives the formation of F-actin protrusions. We demonstrate that endogenous Rab25 vesicles coordinate the positioning of key cargos, including the actin regulator FMNL1 and integrin β1, with the activation of Rho guanosine triphosphatases at the plasma membrane to generate and maintain F-actin-rich filopodium-like protrusions and promote cancer cell invasive migration in the three-dimensional matrix.

This study demonstrates that acute aerobic exercise alters the serum protein profile in CRC patients, with significant reductions in ARF6, ARF5, and RAB11A representing the most meaningful changes. These findings provide strong evidence supporting the use of acute aerobic exercise as a therapeutic intervention for CRC.

Furthermore, we found the underlying mechanism of SNX10 in HER2 traffic by regulating the endosomal RAB11A. We propose that SNX10 deficiency contributes to the inhibition of HER2 recycling as well as the decrease of cell-surface HER2 and causes anti-HER2 ADC resistance.