Meanings of tumor necrosis factor receptor superfamily member 1b precursor in English

The clinical picture resolved after etanercept was withdrawn and treatment with immunosuppressants.

New and continuing patients showed similar results, with etanercept having the lowest costs.

For etanercept the one year data have shown a reduction in x-ray progression.

No increase in toxicity was associated with combination treatment with etanercept plus MTX.

But recently, there's been more interest in injections of immune-suppressing drugs like etanercept.

Deleting p75 from the urothelium prevented urothelial death, but resulted in reduction in overall voiding efficiency after SCI.

The viral integrase protein interacts with transcriptional co-activator lens epithelium-derived growth factor p75 to principally position integration within gene bodies.

The neurotrophin receptor p75 is induced by various injuries to the nervous system, but its role after injury has remained unclear.

We further demonstrate that proNGF binds p75 in vivo and that disruption of this binding results in complete rescue of injured adult corticospinal neurons.

Here, we report that p75 is required for the death of oligodendrocytes following spinal cord injury, and its action is mediated mainly by proNGF.

However, a chimeric receptor in which the DD of CD120a was fused to the cytoplasmic domain of CD120b was predominantly localized to lipid rafts.

Plasma concentration of soluble interleukin-2 receptor and soluble tumor necrosis factor receptor 2 was measured by enzyme-linked immunosorbent assay (ELISA).

The serum marker with the best accuracy to discriminate PCM cases from controls was sTNF-R2.

Late PE had higher levels of sTNF-R1 and sTNF-R2 than early PE.

These results indicate that the sustained expression of TNF-R2 in AM by BLM exposure may sensitize these cells to TNF-a-mediated toxicity.

This induction of TNF-R2 by BLM was significant on d 1 and increased with greater exposure time.

In summary, our data suggest a critical regulatory role of TNF-R2 signaling for disease exacerbation in Th1-mediated chronic colitis.