-
miR-193a-3p is downregulated in ulcerative colitis neoplasia, and its loss promotes carcinogenesis through upregulation of IL17RD. These findings provide novel insight into inflammation-driven colorectal cancer and could suggest new therapeutic targets in this high-risk population
-
Low SEF expression is associated with Epithelial-Mesenchymal Transition in Breast Cancer and thus Metastasis in breast Cancer.
-
Taken together, these data suggest evidence that loss of hSef may be a critical event facilitating tumor dissemination of prostate cancer through alteration of EMT.
-
IL17RD negatively regulates Toll-like receptor (TLR)-induced responses.
-
Demonstrate SEF expression in a healthy ovary during folliculogenesis and suggest hormonal regulation of its expression may be an important factor involved in intra-ovarian control mechanisms.
-
Downregulation of Dusp6, Sprouty4, and Sef--negative modulators of FGF2/ERK1/2 signaling--was present in eutopic endometria of adenomyosis, which may play critical roles in the development of adenomyosis.
-
These results reveal Sef-S actives Lys63-linked TAK1 polyubiquitination on lysine 209, induces TAK1-mediated JNK and p38 activation and also results apoptosis in 293T cells.
-
FGF17 and IL17RD prpopsed as the two top candidates in the entire proteome on the basis of a statistical test of their protein-protein interaction patterns to proteins known to be altered in congenital hypogonadotropic hypogonadism.
-
Downregulation of SEF mRNA is associated with prostate cancer.
-
Orphan receptor IL-17RD tunes IL-17A signalling and is required for neutrophilia.
-
This study establishes Sef as a feedback antagonist of proinflammatory cytokines and highlights its potential to regulate the crosstalk between proinflammatory cytokine receptors and receptor tyrosine kinases.
-
The expression of hSef is decreased in epithelial ovarian carcinoma tissue, but the expression of FGF-2 is increased.
-
Findings indicate that Ras-induced nuclear accumulation of activated MEK1/2 was reliant on downregulation of the spatial regulator Sef.
-
Sef exerts its inhibitory effects at the level of FGFR and upstream of Ras providing an additional level of negative regulation of FGF signaling
-
human SEF is likely to play critical roles in endothelial or epithelial functions such as proliferation, migration, and angiogenesis
-
HSef acts as a spatial regulator for ERK signaling by targeting ERK to the cytoplasm.
-
Sef binds to TAK1 and has a role in JNK activation and apoptosis
-
Sef is downregulated in advanced prostate cancer and might facilitate an enhanced tumorigenic response to FGFs
-
Sef inhibited FGF induced, but not RasG12V mediated, signal transduction. We propose that Sef interacted with Ras in the inhibition of Ras/MAPK signaling pathway.
-
hSef isoforms can control signal specificity and subsequent cell fate by utilizing different mechanisms to modulate RTK signaling