NLRC5 (NLR Family CARD Domain Containing 5)

Mesocolic hyperplasia, closely replicating the key histopathological and molecular features of CD-related CrF, developed in half of the rats in this model. This model provides a cost-effective platform for studying the interplay between intestinal inflammation and mesenteric adipose tissue remodeling.

In this review, we compile and critically review the recent data on NLRX1, highlighting its molecular interactions, signaling pathways, and disease-modulating functional relevance. Integrating findings from recent experimental and clinical research, this review attempts to discern the general biological significance of NLRX1 as well as its promise as an emerging therapeutic target in the new era of advanced research.

We further identify low-abundance asymmetric SAMD9 dimers in which one protomer undergoes large conformational changes and establishes intermolecular interactions that are essential for SAMD9 activation. Together, these findings define the structural basis of SAMD9 autoinhibition and explain how human GoF mutations subvert this regulatory mechanism to drive disease.

In PMLs, basal cells with high levels of NLRC5 were in close spatial proximity to CD8+ T cells, suggesting that these cells exhibit increased functional MHC-I gene expression in vivo. These findings indicate a functional role for hsa-miR-149-5p in PML progression/persistence and suggest this axis as a potential therapeutic target for PML immunomodulation.

Kupffer cells treated with ALA (100 μM) prior to LPS stimulation significantly enhanced glucose uptake and upregulated the expression of insulin signaling related proteins, including phosphorylated phosphoinositide 3-kinase (p-PI3K), phosphorylated protein kinase B (p-Akt) and glucose transporter type 2 (GLUT2) expression, in FL83B hepatocytes cultured with a conditioned medium from LPS-primed and ATP/nigericin-stimulated Kupffer cells (p < 0.05). These findings highlight the potential of ALA as a modulator of hepatic immune-metabolic interactions and support its therapeutic relevance for managing insulin resistance in T2DM.

Complementary transcriptomic analysis using a compact four-gene Tα1 Response Index (Tα1-RI: TLR9, TLR2, IRF1, NLRC5) in TCGA-BRCA (n = 1,112) confirmed positive correlations with antigen presentation and cytotoxic programs and enrichment in CD8-like T cells in single-cell datasets. Collectively, these findings demonstrate that Tα1 enhances CD8+ T cell cytotoxicity while alleviating exhaustion, supporting its potential as an adjunct immunomodulator for improving immune surveillance in breast cancer.

Pharmacological inhibition of FAK with single agent VS-4718 did not significantly reduce macroscopic tumor volume; however, its use in combination with the mitogen-activated protein kinase kinase (MEK) inhibitor selumetinib resulted in both a significant reduction in tumor volume and the preservation of dorsal root ganglion architecture. Our findings establish a critical role for FAK in schwannoma development and provide rationale for evaluation of combination FAK plus MEK inhibition in future clinical trials for NF2-associated SWN.

Clinically, elevated serum levels of soluble MerTK (s-Mer) correlated with hepatic injury severity and Caspase-1 activation in patients after partial hepatectomy or liver transplantation. Our findings suggest a potential therapeutic strategy for LIRI prevention and treatment.

In conclusion, GA activates the Hippo pathway and promotes YAP1 translocation to the cytoplasm, leading to its degradation and subsequent inhibition of PSC activation and fibrosis. These findings highlight the critical role of ubiquitin-mediated YAP1 degradation in regulating PSC activity and offer novel insights into the therapeutic potential of GA for treating pancreatic fibrosis.

NCHBL-005 and its metabolite indole-3-acetaldehyde alleviate psoriatic inflammation through modulation of the aryl hydrocarbon receptor-interleukin-1 beta-interleukin-17A axis, thereby restoring skin immune homeostasis. This study highlights postbiotic intervention in the aryl hydrocarbon receptor-interleukin-1 beta-interleukin-17A axis as a promising therapeutic strategy for psoriasis.

Genetic and pharmacological evidence demonstrated that NOD2 is essential for aripiprazole-induced pyroptosis and downstream signal propagation. This study provides mechanistic insight into the anti-cancer potential of aripiprazole and supports the broader investigation of serotonergic drugs as immunomodulatory agents in cancer therapy.

Shengmai San effectively attenuates irradiation-induced salivary gland hypofunction and fibrosis, mainly through inhibition of the SPHK1-S1P-S1PR1 signaling pathway.