IL1RAP (Interleukin 1 Receptor Accessory Protein)

In vivo experiments confirmed that low-dose GCP intervention significantly reduced intestinal hemorrhage and edema, decreased parasite loads in intestinal and cerebral tissues of infected mice, and suppressed protein expression of IL-17RA, TNF-α, p-C/EBPβ and p-NF-κB in intestinal tissues. These findings demonstrate that GCP mitigates NC-induced IEC injury by modulating intestinal immune homeostasis through the C/EBPβ/IL-17/TNF signaling pathway, thus establishing a theoretical basis for developing natural therapeutics against pathogen-induced gut damage.

Critically, pharmacological inhibition abolished GGPPS-driven geranylgeranylation-dependent signaling: JSH-23 reversed both the proliferation mediated by RHOA and NF-κB p65 and the upregulation of IL1B potentiated by GGPS1 overexpression; and NSC23766 blocked the RAC1/STAT1-dependent IL1RAP activation amplified by GGPPS elevation, confirming that both axes are indispensable for GGPPS-dependent proliferation. Collectively, this GGPPS-mediated geranylgeranylation axis, converging on IL-1 pathway amplification, represents a central therapeutic vulnerability in LUSC, highlighting GGPPS as a promising macromolecular target for this recalcitrant malignancy.

Functional assays demonstrated that GHR overexpression suppressed proliferation, migration, and invasion while promoting apoptosis. Our study integrates bulk and single-cell transcriptomics with functional validation, unveiling cytokine-driven mechanisms in HBV-HCC. The cytokine-based prognostic model holds promise for risk stratification, immunomodulation, and personalized therapy, offering new avenues for improving HBV-HCC management.

It also reduced AML engraftment in leukemic mice. Our findings highlight the therapeutic potential of UR241-2 in targeting IL-1/IRAK1/4 signaling to eradicate LSCs and improve AML outcomes.

Methylation analyses indicated complex regulation of CTSS and TNFRSF19. WFDC1, RHOC, and GSTM4 exhibit therapeutic potential, while MFGE8, CTSS, TNFRSF19, and IL1RAP predict risk and prognosis, providing insights for precision diagnosis and treatment.

Using a mouse model of CH, they connect the clonal expansion triggered by World Trade Center particulate matter exposure to higher levels of IL1RAP, offering a new potential target to limit clonal expansion and reduce CH-associated risks. See related article by Verma et al., p. 2468.

Because PTPRD functions are pathway-specific and shaped by mini-exon usage or redundancy with other family members (PTPRS/PTPRF), domain- or ligand-selective interventions represent plausible therapeutic strategies. Elucidating its full ligand repertoire, substrate landscape, and structural basis for allosteric regulation will be critical for converting this versatile receptor from a mechanistic curiosity into a tractable target for neurodevelopmental, neuropsychiatric, and metabolic disorders.

We have identified a potentially novel strategy to enhance CAR-T cell persistence and efficacy in AML by counteracting a leukemia-induced, microRNA-deficiency mediated mechanism of immune suppression.

These results highlight potential cytokine and chemokine-mediated pathways involved in melanoma dermal invasion and cutaneous metastasis. While some findings did not reach statistical significance, concordant trends between in vitro and patient-derived data suggest their relevance and warrant further investigation in larger cohorts.

Inflammation sensor, IL1RAP, was overexpressed in murine CH, and genetic knockdown inhibited mutant clone growth in-vivo. This study links discrete environmental exposure to hematopoietic mutations and leukemia, identifying IL1RAP as a novel therapeutic target in CH.

Computational studies revealed strong binding affinities with six proteins associated with cancer, positive pharmacokinetic properties, and no toxicity. Our contribution suggests that IA may be a compound with potential therapeutic effects against NHL.

The results of the present study further elucidated the molecular processes underlying PDAC and highlight the crucial importance of manganese metabolism in its development. These biomarkers may provide significant prognostic insights and facilitate the advancement of targeted therapeutic strategies for PDAC.