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Protein Page:
STXBP4 (human)
p Phosphorylation
a Acetylation
m Methylation
m1 Mono-methylation
m2 Di-methylation
m3 Tri-methylation
u Ubiquitination
s Sumoylation
n Neddylation
gl O-GlcNAc
ga O-GalNAc
h Palmitoylation
ad Adenylylation
sn S-Nitrosylation
ca Caspase cleavage

Overview
STXBP4 Plays a role in the translocation of transport vesicles from the cytoplasm to the plasma membrane. Inhibits the translocation of SLC2A4 from intracellular vesicles to the plasma membrane by STX4A binding and preventing the interaction between STX4A and VAMP2. Stimulation with insulin disrupts the interaction with STX4A, leading to increased levels of SLC2A4 at the plasma membrane. May also play a role in the regulation of insulin release by pancreatic beta cells after stimulation by glucose. Interacts with STX4A. 2 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Vesicle protein
Cellular Component: intermediate filament cytoskeleton; cytoplasm; nucleolus; nucleus
Molecular Function: calcium ion binding
Biological Process: insulin receptor signaling pathway; glucose transport; protein targeting
Reference #:  Q6ZWJ1 (UniProtKB)
Alt. Names/Synonyms: FLJ16496; MGC149829; MGC50337; STX4-interacting protein; STXB4; STXBP4; Synip; syntaxin 4 interacting protein; Syntaxin 4-interacting protein; syntaxin binding protein 4; Syntaxin-binding protein 4
Gene Symbols: STXBP4
Molecular weight: 61,662 Da
Basal Isoelectric point: 5.12  Predict pI for various phosphorylation states
CST Pathways:  Insulin Receptor Signaling
Protein-Specific Antibodies or siRNAs from Cell Signaling Technology® Total Proteins
Select Structure to View Below

STXBP4

Protein Structure Not Found.


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Modification Sites and Domains Show Modification Legend
Click here to view phosphorylation modifications only

Modification Sites in Parent Protein, Orthologs, and Isoforms Show Modification Legend
 

Show Multiple Sequence Alignment


 SS 

SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.


 MS 

MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.


       human

► Hide Isoforms
 
0 1 T5 ___MNKNTsTVVsPs
0 2 S6-p __MNKNTsTVVsPsL
0 4 S10-p KNTsTVVsPsLLEkD
0 2 S12-p TsTVVsPsLLEkDPA
0 1 K16-u VsPsLLEkDPAFQMI
0 1 K27-u FQMITIAkETGLGLK
3 3 S99-p GAKLRLEsAWEIAFI
0 3 T157-p KTSSTPKtNNDILSS
0 1 S208 YGLQEKISLNPsVRF
0 1 S212-p EKISLNPsVRFKAEK
0 1 K385-u EAKITELkAQLADYS
0 1 K396-u ADYSDQNkESVQDLK
0 4 T446-p EVFSDNStPLSNLSE
0 1 S460-p ERRAVLAsQTsLtPL
0 2 S463-p AVLAsQTsLtPLGRN
0 1 T465-p LAsQTsLtPLGRNGR
  STXBP4 iso2  
- gap
- gap
- gap
- gap
- gap
- gap
S24 KLSTRLESAWEIAFI
T82 KTSSTPKTNNDILSS
S133 YGLQEKISLNPSVRF
S137 EKISLNPSVRFKAEK
- gap
- gap
- gap
- gap
- gap
- gap
  mouse

 
T5-p ___MSDGtASARSSs
- gap
S10 DGtASARSSsPLDRD
S12-p tASARSSsPLDRDPA
R16 RSSsPLDRDPAFRVI
K27 FRVITVTKETGLGLK
S99-p RAKLRSEsPWEIAFI
T156 KTSSTPQTQDSTFPS
S212-p SGPQGKIsLNPSVRL
S216 GKIsLNPSVRLKAEK
K389 EAEVSELKAQLADYS
K400 ADYSDQNKESVQDLR
- gap
S464 ERRAVLASQTSLPLL
S467 AVLASQTSLPLLARN
- gap
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