CNTFR (Ciliary Neurotrophic Factor Receptor)

SWS is a rare autosomal recessive disorder characterized by autonomic dysfunction and bent-bone dysplasia due to pathogenic homozygous or compound heterozygous variants in the LIFR gene. Management is currently supportive, and further research is required to improve treatment and prognosis.

The LIFR protein interaction network was also predicted and found to interact with the reported ciliary neurotrophic factor (CNTF), cardiotrophinlike cytokine factor 1 (CLCF1), interleukin 6 cytokine family signal transducer (IL6ST), and ciliary neurotrophic factor receptor (CNTFR) proteins. In conclusion, the c.*127 T>C locus of LIFR gene can be used as a candidate genetic molecular marker to increase lambing numbers in polytocous sheep.

CNTFR is a promising noninvasive diagnostic biomarker for prostate cancer. Its reduced expression in urine and tissues, along with its association with poor prognosis, highlights its potential for improving prostate cancer diagnosis and outcomes through noninvasive methods.

As a result, no toxicity related CLCF1 proteins was observed based on the behavior sign observation and body weight changes. In conclusion, we successfully established the strategies of production and characterization of biologically active recombinant CLCF1 proteins in mammalian cells as potential biotherapeutics.

Furthermore, the tested extracts showed a potential to alter the mRNA of various genes, including Zfp91, B2m, Nr3c1, Insr, Atrn, Il6ra, Hsp90ab1, Sort1, and Npy1r. In conclusion, the data generated from the current study suggested that the two extracts under investigation are considered potential candidates for controlling insulin levels and managing obesity.

Moreover, syngeneic mouse models showed that the murine surrogate of C5252 has superior anti-tumor activity compared to the unarmed backbone virus, with enhanced immune activation. Taken together, our findings support C5252 as a promising therapeutic option for glioblastoma treatment, positioning it as a highly promising candidate for clinical translation.

By re-evaluation of IC7 and CNTF, we discovered the Oncostatin M receptor (OSMR) as an alternative non-canonical high-affinity receptor leading to IL-6R:OSMR:gp130 and CNTFR:OSMR:gp130 receptor complexes, respectively. The discovery of OSMR as an alternative high-affinity receptor for IC7 and CNTF designates GIL-6 as the first truly selective IL-6R:gp130:LIFR cytokine, whereas GIO-6 is a CNTF-free alternative for IC7.

Our work suggests a role for IFN-γ in PD-L1 upregulation in OPMC and presents novel IO transcriptional signatures for frankly invasive OSCC relative to TM.

In this study, we integrated ultra high-plex single-cell spatial transcriptomics, optimal transport ligand-receptor predictions, and genetically-engineered stromal tumoroids to identify and validate CLCF1-CNTFR as an important intercellular mechanism of resistance to chemoradiotherapy in PDAC-pioneering a paradigm for translating single-cell spatial biology to clinical oncology.

It was found that there were two binding sites of miR-708 and CNTFR, 394-400 bp and 497-503 bp respectively. In conclusion, miR-708 can reduce the expression of CNTFR by binding to the target gene CNTFR3' UTR, activate the JAK/STAT pathway to regulate apoptosis-related proteins, reduce apoptosis, and enhance the migration ability of leukemia cells.

External validation of the only available m6A sequencing in ccRCC consistently reduced dysregulated m6A-driven targets on the NNU panel with highly significant effects on OS. Epitranscriptomics are a promising target for developing novel therapies and for identifying prognostic markers for daily clinical practice.