Accession | Acc. Gene-, Name | Start | End | Subsequence | Logic | PDB | Organism | Length |
---|---|---|---|---|---|---|---|---|
ELMI001222 | Q9Y2N7 HIF3A HIF3A_HUMAN |
490 | 502 | LEMLAPYISMDDDFQLNASE | TP | --- | Homo sapiens (Human) | 669 |
Instance evidence
Evidence class | PSI-MI | Method | BioSource | PubMed | Logic | Reliability | Notes |
---|---|---|---|---|---|---|---|
experimental | MI:0019 | coimmunoprecipitation | in vivo/in vitro | Maynard,2003 | support | likely | InteractionDetection |
experimental | MI:0101 | sequence based prediction | in silico | Maynard,2003 | support | certain | InteractionDetection |
Switches
This ELM instance is part of the following 2 switching mechanisms annotated at the switches.ELM resource:
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SWTI000026:
Hydroxylation of P492 in the VHL-binding motif of Hypoxia-inducible factor 3-alpha (HIF3A) induces binding to the Von Hippel-Lindau disease tumor suppressor (VHL) protein.
-
SWTI000581:
Alternative splicing removes the VHL-hydroxyproline-modified binding motif of Hypoxia-inducible factor 3-alpha (HIF3A), abrogating binding to Von Hippel-Lindau disease tumor suppressor (VHL). Other studies have shown that the HIF-3 alpha-4 splice variant (Isoform HIF-3alpha4) can act as a dominant negative form with tumour-suppressive activity (see Maynard et al. (2007) (here)).
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