BST1/YFL025C Summary 
| Standard Name | BST1 (see Nomenclature conflict Note) |
|---|---|
| Systematic Name | YFL025C |
| Alias | PER17 1 |
| Feature Type | ORF, Verified |
| Description | GPI inositol deacylase of the ER that negatively regulates COPII vesicle formation, prevents production of vesicles with defective subunits, required for proper discrimination between resident ER proteins and Golgi-bound cargo molecules (2, 3 and see Summary Paragraph) |
| Name Description | Bypass of Sec Thirteen 3 |
| Chromosomal Location | |
|---|---|
| Note: this feature is encoded on the Crick strand. | |
|
| View Computational GO annotations for BST1 | |
| Molecular Function | |
| Manually curated | |
| Biological Process | |
| Manually curated | |
| Cellular Component | |
| Manually curated | |
| High-throughput |
| 351 total interaction(s) for 192 unique genes/features. | |
| Physical Interactions |
|
| Genetic Interactions |
|
| Resources |
|
|
| |
| Resources |
| Localization | |
|---|---|
| Phosphorylation | PhosphoGRID | PhosphoPep Database |
| Structure | |
| Homologs |
| Note: this feature is encoded on the Crick strand. | |||||||||||||
|
| |||||||||||||
| Last Update | Coordinates: 2011-02-03 | Sequence: 1996-07-31 | ||||||||||||
| Subfeature details |
| ||||||||||||
| Retrieve sequences | |||||||||||||
| S288C only | |
|---|---|
| S288C vs. other species | |
| S288C vs. other strains |
| External Links | All Associated Seq | E.C. | Entrez Gene | Entrez RefSeq Protein | MIPS | Search all NCBI (Entrez) | UniProtKB |
|---|
| Primary SGDID | S000001869 |
|---|
NOMENCLATURE CONFLICT NOTE
| Name | Relevance | Description |
|---|---|---|
| DPL1 | Nomenclature conflict | Both YDR294C/DPL1 and YFL025C/BST1 have been referred to as BST1. |
Bst1p is a glycosylphosphatidylinositol (GPI) inositol deacylase that mediates inositol deacylation of GPI-anchored proteins, which may be required for their efficient incorporation into COPII transport vesicles through association with cargo receptors (3). An integral membrane protein that resides predominantly in the endoplasmic reticulum (ER), Bst1p negatively regulates COPII vesicle formation, preventing the production of vesicles with defective or missing subunits (1). Bst1p is also required for proper discrimination between resident ER proteins and Golgi-bound cargo molecules (2), and is required for the transport of misfolded proteins to the Golgi, though dispensable for the transport of many normal cargo proteins (1). Bst1p also plays a role in the retrieval to the ER of proteins transported to the Golgi apparatus via COPII-coated vesicles. Bst1p thus represents a novel class of ER proteins that link the regulation of vesicle coat assembly to cargo sorting (2). Null mutations in BST1 suppress mutations in the essential COPII gene SEC13, which is important for the formation of ER to Golgi transport vesicles (2).
Last updated: 2004-11-02 
| 1) | Vashist S, et al. (2001) Distinct retrieval and retention mechanisms are required for the quality control of endoplasmic reticulum protein folding. J Cell Biol 155(3):355-68 |
| 2) | Elrod-Erickson MJ and Kaiser CA (1996) Genes that control the fidelity of endoplasmic reticulum to Golgi transport identified as suppressors of vesicle budding mutations. Mol Biol Cell 7(7):1043-58 |
| 3) | Tanaka S, et al. (2004) Inositol deacylation of glycosylphosphatidylinositol-anchored proteins is mediated by mammalian PGAP1 and yeast Bst1p. J Biol Chem 279(14):14256-63 |
