| Accession | Acc. Gene-, Name | Start | End | Subsequence | Logic | PDB | Organism | Length |
|---|---|---|---|---|---|---|---|---|
| ELMI002451 | Q969H0 FBXW7 FBXW7_HUMAN |
202 | 207 | STTGLVPCSATPTTFGDLRA | TP | --- | Homo sapiens (Human) | 707 |
Instance evidence
| Evidence class | PSI-MI | Method | BioSource | PubMed | Logic | Reliability | Notes |
|---|---|---|---|---|---|---|---|
| experimental | MI:0096 | pull down | in vivo/in vitro | support | certain | InteractionDetection | |
| experimental | MI:0519 | glutathione s tranferase tag | in vitro | Min,2012 | support | certain | |
| experimental | MI:0007 | anti tag coimmunoprecipitation | in vivo | Min,2012 | support | certain | InteractionDetection |
| experimental | MI:0019 | coimmunoprecipitation | in vivo/in vitro | Min,2012 | support | certain | InteractionDetection |
| experimental | MI:0074 | mutation analysis | in vivo/in vitro | Min,2012 | support | certain | FeatureDetection |
Switches
This ELM instance is part of the following 1 switching mechanism annotated at the switches.ELM resource:
-
SWTI000661:
Phosphorylation of T205 in the Pin1-binding motif of F-box/WD repeat-containing protein 7 (FBXW7) induces binding to the Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1) protein. Pin1 interacts with Fbw7 in a phoshorylation-dependent manner and promotes Fbw7 self-ubiquitination and protein degradation by disrupting Fbw7 dimerization. Paper also shows the over-expression of Pin1 suppresses the ability of Fbw7 to inhibit cell transformation and proliferation, suggesting a link between Pin1 overexpression and cancer.
Pathways
Please cite:
ELM-the Eukaryotic Linear Motif resource-2024 update.
(PMID:37962385)
ELM data can be downloaded & distributed for non-commercial use according to the ELM Software License Agreement
ELM data can be downloaded & distributed for non-commercial use according to the ELM Software License Agreement