Publication for Nf1 and Spred1
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Nf1 | neurofibromin 1 | 18015 | [link] | ||
| mmu | Spred1 | sprouty protein with EVH-1 domain 1, related sequence | 114715 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 23443682 | 0.98 | SPRED1) recruits NF1 to membranes and is required for NF1 to inactivate Ras in cell lines. |
| 0.98 | SPRED1 engages NF1 and an N-terminal Sprouty (SPR) domain allows membrane localization of the SPRED1-NF1 complex, most likely through interaction with phospholipids and caveolin 1 (Fig. 2B). | |
| 0.98 | NF1 to membranes and, therefore, its targeting to Ras is mediated by SPRED1 in some cell types. | |
| 0.98 | NF1 binds membranes in these cell types through recognition of SPRED2 or SPRED3, proteins that are homologous to SPRED1. | |
| 0.98 | NF1 to membranes in the absence of SPRED1. | |
| 0.98 | NF1 can be targeted to membranes through an undefi ned interaction with the SPRED1 protein that binds to membrane lipids through its SPR domain. | |
| 0.95 | SPRED1 mutations are nonsense mutations that lack the SPR domain, which results in the loss of membrane localization of NF1 in cultured cells. | |
| 0.87 | NF1 protein region is recognized by the EVH domain and whether or not the SEC14-PH domain of NF1 cooperates with SPRED1 in membrane targeting is not known. | |
| 19186160 | 0.98 | NF1 or SPRED1 result in elevation of ERK pathway activation. |
| 0.96 | SPRED1 gene product normally acts to suppress ERK activation, as does NF1. | |
| 0.76 | NF1-like syndrome, which results from loss-of-function mutations in the SPRED1 gene. | |
| 24183794 | 0.98 | SPRED-1 targets the neurofibromin-1 (NF1) RasGAP to membranes, thereby allowing NF1 to inactivate Ras. |
| 0.96 | NF1, and that loss of membrane targeting of these other RasGAPs underlies the increased MAPK activation in SPRED1/2 deficient LEC, although this remains to be determined. | |
| 23312374 | 0.97 | Nf1+/- mice, defective spred1 function in mice resulted in increased MAPK signaling, in addition to deficits in learning and memory. |
| 29301958 | 0.97 | Nf1, Dusp6, Spred1, Rasa2, and SPOP (Fig. 1D). |
| 29079424 | 0.96 | neurofibromin suggests that these isoforms may compensate for loss of Spred1 and thus helps explain the milder phenotype associated with NFLS in comparison with NF1. |
| 0.95 | NF1 are explained by the shared underlying molecular mechanism: SPRED1 downregulates the RAS/MAPK pathway through neurofibromin, the NF1 gene product. | |
| 0.85 | SPRED1 cause Neurofibromatosis Legius syndrome (NFLS), a mild form of Neurofibromatosis 1 (NF1), which is characterized by multiple cafe-au-lait skin spots, variable dysmorphic features such as hypertelorism or macrocephaly, lipomas, and mild learning disabilities or attention problems (Figure 5A). | |
| 20345245 | 0.93 | Nf1, lossof- function mutations of SPRED1 also result in hyperactivity in MEK/MAPK signaling. |
| 0.53 | Spred1 mutations involves some of the same symptom dimensions (other than neurofibromas) seen in NF1. | |
| 28455524 | 0.91 | Nf1 , Ptpn11 , Spred1 mice and conditional Kras G12V mice. |
| 0.90 | NF1, SPRED1, PTPN11 and KRAS which diverge in their relative subcellular signaling mechanisms. | |
| 22821737 | 0.79 | Spred1 knockout mice revealed hippocampal synaptic plasticity and learning deficits similar to those previously described in Nf1+/- heterozygous mice. |
| 25393061 | 0.77 | Nf1 and Spred1 mouse models, inhibitor treatment may also be beneficial for learning issues in an animal model for NS. |
| 21495177 | 0.61 | Spred1-/- mice is remarkably similar to that in Nf1+/- mice. |
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