High impact information on Il17rd

• Therefore, alternative splicing of the hSef gene expands the Sef feedback inhibition repertoire of RTK signaling [1].
• Sef was recently identified as a negative regulator of fibroblast growth factor (FGF) signaling in a genetic screen of zebrafish and subsequently in mouse and humans [2].
• Furthermore, our data suggested Sef exerted the negative effect on FGF2-induced PC-12 cell differentiation through the prevention of Ras-mitogen-activated protein kinase signaling, possibly functioning upstream of the Ras molecule [3].
• We provide evidence that the Sef gene products were located mainly on the cell membrane [3].
• By repressing events upstream and/or downstream Ras, Sef inhibits FGF-induced ERK activation and cell proliferation [4].

Biological context of Il17rd

• Using bioinformatic methods and rapid amplification of cDNA ends-PCR, we isolated both the mouse and the human Sef genes, which encoded the Sef protein and Sef-S isoform that was generated through alternative splicing [3].
• These findings suggest that Sef may play an important role in the regulation of PC-12 cell differentiation [3].
• Cloning of the mouse Sef gene and comparative analysis of its expression with Fgf8 and Spry2 during embryogenesis [5].
• Sef-S inhibits FGF-induced NIH3T3 cell proliferation, a similar function to Sef [4].

Anatomical context of Il17rd

• Altogether, our results demonstrate that Sef and Sproutys function synergistically to regulate Gbx2 expression in the anterior hindbrain [6].
• Expression of Sef is similar to that of Fgf8 and Spry2 during early embryogenesis, being prominent in the forebrain, mid-hindbrain boundary, branchial arches, somites, limb bud and tailbud of mouse embryos [5].
• Here we report that Sef-S, an alternative splice isoform of Sef, lacks a signal peptide and is localized in cytosol [4].

Regulatory relationships of Il17rd

• Synergistic activity of Sef and Sprouty proteins in regulating the expression of Gbx2 in the mid-hindbrain region [6].

References