| Accession | Acc. Gene-, Name | Start | End | Subsequence | Logic | PDB | Organism | Length |
|---|---|---|---|---|---|---|---|---|
| ELMI002596 | P78381 SLC35A2 S35A2_HUMAN |
392 | 396 | RGDLITEPFLPKLLTKVKGS | TP | --- | Homo sapiens (Human) | 396 |
Instance evidence
| Evidence class | PSI-MI | Method | BioSource | PubMed | Logic | Reliability | Notes |
|---|---|---|---|---|---|---|---|
| experimental | MI:0416 | fluorescence microscopy | Kabuss,2005 | support | likely | InteractionDetection | |
| experimental | MI:0074 | mutation analysis | in vivo/in vitro | Kabuss,2005 | support | likely | FeatureDetection |
Switches
This ELM instance is part of the following 1 switching mechanism annotated at the switches.ELM resource:
-
SWTI000522:
Alternative splicing removes the di-lysine ER-retention motif of UDP-galactose translocator (SLC35A2), abrogating binding to Coatomer subunit alpha (COPA). This motif localises Isoform UGT1 exclusively in the Golgi whereas Isoform UGT2 shows dual expression in both the Golgi and the ER. This motif is considered a weak retention signal.
Please cite:
The Eukaryotic Linear Motif resource: 2022 release.
(PMID:34718738)
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