CUSABIO Quarterly Citation Review: 800 New Product Citations in Q3, Total Citations Hit 27,500!

This study shows that the FAK/SFK axis drives ESCC lymph node metastasis via tyrosine phosphorylation of metabolic enzymes ACLY and ALDOA, enhancing their activity and activating CDK7/9 or Yamanaka factors in primary vs. metastatic tumors. The natural compound quercetagitrin selectively inhibits ALDOA phosphorylation, suppressing metastasis and synergizing with FAK/SFK inhibitors, offering a promising anti-metastatic strategy.

This study identified rare loss-of-function TRAF5 variants in 3.78% of SLE-PAH patients from the CSTAR cohort. TRAF5 deficiency exacerbated pulmonary vascular remodeling in mouse models, with single-cell RNA-seq revealing downregulated TRAF5 in arterial endothelial cells, disrupted BMP/TGF-β signaling, and increased apoptosis. Endothelium-specific TRAF5 overexpression attenuated PAH in model mice, highlighting its therapeutic potential.

This study presents a bioactive iron-chelating PACG/CS hydrogel scaffold that orchestrates a dual hypoxic-immune microenvironment for functional meniscus regeneration. By chelating Fe³⁺ ions, the scaffold activates HIF-1α signaling, induces a hypoxic niche, and modulates macrophage polarization, enhancing stem cell recruitment and chondrogenic differentiation. Peripheral blood-derived MSCs (PBMSCs) showed superior regenerative potential compared to bone marrow MSCs (BMSCs). Combined with personalized 3D printing, the scaffold reconstructed heterogeneous meniscal structures, restored biomechanical properties, and protected articular cartilage in vivo.

This study shows nasal Staphylococcus aureus promotes depressive behavior in mice by secreting 17β-HSD (Hsd12) to degrade sex hormones, reducing brain dopamine and serotonin. The effect is stronger in females, revealing a novel nose–brain axis mechanism in depression.

This study shows oral commensal Veillonella parvula enriches in Crohn’s disease (CD) gut and worsens Clostridioides difficile infection (CDI). Its LPS triggers TLR4-MAPK-c-Jun/c-Fos signaling, suppresses ileal bile acid transporter ASBT, increases luminal bile acids, and promotes spore germination and recurrence, offering a novel therapeutic target for CDI in CD.

This study maps human protein interactomes of ancestral and variant SARS-CoV-2 across organ-specific cells and saliva, revealing NSP3-induced coagulation defects via fibrinogen binding and immune evasion through IFIT5 de-ISGylation. Three antiviral peptides targeting the RBD were developed, effectively blocking ACE2 binding and inhibiting infection by both ancestral and variant strains, offering promising broad-spectrum antiviral candidates.

This study employs AI to identify bufalin as a molecular glue that degrades ERα by enhancing its interaction with E3 ligase STUB1, promoting proteasomal degradation. Bufalin selectively binds to Arg394 of ERα, suppresses ER+ breast cancer cell growth, and overcomes tamoxifen resistance in vitro, in vivo, and in patient-derived organoids, offering a promising therapeutic strategy with favorable safety.

Using SIV-MPXV co-infected macaques to mimic HIV-mpox co-infection, this study shows co-infection worsens skin lesions, increases multi-organ viral loads, and impairs CD8+T cell and neutralizing antibody responses. Proteomic/phosphoproteomic analyses reveal activated immune-inflammatory pathways, viral exploitation of cell cycle/DNA replication, and CDK-PLK axis as a potential therapeutic target, offering key insights for co-infection mechanisms and interventions.

This study reveals RKIP regulates bone homeostasis by directing bone marrow macrophage fate: cytoplasmic RKIP binds ARHGAP to prevent CDC42 inactivation, enhancing osteoclastogenesis, while nuclear RKIP bridges VHL and HIF-1α to promote its degradation, suppressing angiogenesis. RKIP deletion or inhibition reduces osteoclasts, increases pro-angiogenic macrophages, boosts H-type vessel formation, markedly elevates bone mass, and rescues ovariectomy-induced osteoporosis, offering a novel therapeutic target.

Prenatal propylparaben exposure triggers transgenerational DOR in mice via persistent Rhobtb1 hypomethylation in oocytes, elevating RhoBTB1 to de-repress FGF18 through ubiquitination, activating MAPK and granulosa apoptosis; similar hypomethylation occurs in DOR patients' blood. Methyl-donor diet rescues F1–F3 phenotypes, revealing DOR as an inheritable epigenetic disorder and offering non-invasive biomarkers and nutritional intervention strategies.