RAB5A (Ras-related protein Rab-5A)

Overexpression of dominant-negative Rab4 or Rab5 has a similar inhibitory effect on neutrophil migration. Our data suggest that RABAPTIN drives endosomal recycling, Rac activation, and leading-edge actin polymerization, providing significant insights into the role of the endocytic pathway in neutrophil motility.

The presence of DAO in peroxisomes, autophagosomes, lysosomes, and exosomes indicated diverse intracellular localization within CPECs. This distribution may enable efficient metabolism of blood-derived D-serine in CPECs.

TDP-43 co-pathology has a profound effect on AD pathogenesis that may be intrinsically linked to a disruption of the endolysosomal pathway in neurons. Exploring the consequences of TDP-43 dysfunction in the brain can open new avenues for AD biomarker and therapeutic development.

Increasing knowledge of HPX biology will elucidate the causes that regulate plasma HPX, thus improving clinical and veterinary care. Interestingly, increased understanding of the hematological adaptations to weightlessness that lead to anemia, termed "space anemia," in astronauts and space tourists may provide new insights into HPX's role in maintaining iron homeostasis and red cell biology under microgravity conditions as well as upon recovery from space and other anemias.

These findings establish that ATP7B is a critical modulator of sEV cargo and resistance propagation. Our results highlight a previously unrecognized ATP7B-sEV axis driving chemoresistance and identify sEV inhibition as a promising strategy to overcome therapeutic failure in HNSC.

Focusing on two inhibitors, we demonstrate the inhibition of K-Ras in downstream signaling and cellular proliferation in human pancreatic and non-small cell lung cancer cells expressing wild-type or mutant K-Ras. These two compounds represent novel pan-Ras superfamily inhibitors as they also inhibited GTP binding to other members such as RAB5A and RAB35.

These findings demonstrate that Rab5's GTPase cycle is a critical regulator of LD dynamics in HCC cells, governing LD turnover to sustain mitochondrial energy production and support cancer cell proliferation. Targeting the Rab5-mediated regulation of LD metabolism may represent a novel therapeutic strategy to disrupt the metabolic adaptations that fuel liver cancer progression.

Our results revealed considerable variations in RIN3 expression across tumors, an inverse relationship with CNVs and DNA methylation, and a significant correlation with immunotherapy biomarkers. These findings suggest RIN3 as a promising biomarker and therapeutic target, particularly for BRCA-mutated cancers, and may guide the development of novel anticancer strategies.

Additionally, Rabankyrin-5 acts as a dynein adaptor, directly binding both the HPV minor capsid protein L2 and the dynein motor complex to link virus-carrying early endosomes to the dynein transport machinery, thereby promoting virus movement along microtubules. These dual functions enable the coordinated integration of endosomal fusion with microtubule-based transport during the early stages of viral entry.

Furthermore, a combination of Brillouin microscopy and 2.5D traction force analysis reveals a mechanical switch within the spheroid core, characterized by significant cell softening and a reduction in compressive forces exerted on the substrate, thereby mimicking the wetting of a liquid droplet. These findings establish unjamming-driven active wetting as a key mechanism to comprehend the molecular and biophysical underpinnings of solid tumor invasion.

These findings collectively suggest that phagocytic uptake of EBV-infected lymphocytes or their components may serve as a primary infection mechanism for ECs, potentially establishing an immunosuppressive microenvironment that contributes to tumor progression and poor clinical outcomes, though the exact molecular pathways require further elucidation.IMPORTANCEClinical investigations of NPC specimens identified EBERs-positive endothelial cells as clinically significant biomarkers, demonstrating robust correlations with lymphatic metastasis (P < 0.05), distant metastasis (P < 0.01), and advanced tumor staging (P < 0.01), while immunological profiling of affected patients revealed concomitant reductions in B-cell populations (P < 0.01), collectively indicative of systemic immunoregulatory status. Furthermore, integrative experimental approaches incorporating live-cell dynamic imaging, single-cell transcriptional profiling, and ultrastructural electron microscopy provided compelling evidence that endothelial phagocytosis of lymphocytes serves as a principal route for EBV cellular entry and subsequent modulation of the NPC tumor microenvironment.

Consequently, HDAC3 inhibition in BMSCs decreases AML proliferation and synergizes with the anti-AML efficacy of venetoclax. Therefore, our study suggests that targeting HDAC3 in BMSCs may be used for the combination therapy of AML by remodeling the AML-supportive niche.