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Protein Page:
ITM2B (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
ITM2B Plays a regulatory role in the processing of the beta- amyloid A4 precursor protein (APP) and acts as an inhibitor of the beta-amyloid peptide aggregation and fibrils deposition. Plays a role in the induction of neurite outgrowth. Functions as a protease inhibitor by blocking access of secretases to APP cleavage sites. Defects in ITM2B are a cause of cerebral amyloid angiopathy ITM2B-related type 1 (CAA-ITM2B1). A disorder characterized by amyloid deposition in the walls of cerebral blood vessels and neurodegeneration in the central nervous system. Cerebral amyloid angiopathy, non-neuritic and perivascular plaques and neurofibrillary tangles are the predominant pathological lesions. Clinical features include progressive mental deterioration, spasticity and muscular rigidity. ABri amyloidogenic peptide variant is cleaved at the normal furin processing site to generate peptide that accumulates in the brain and produces amyloid fibrils responsible for neuronal dysfunction and dementia. ABri peptide variant forms fibrila in vitro. Defects in ITM2B are a cause of cerebral amyloid angiopathy ITM2B-related type 2 (CAA-ITM2B2); also known as heredopathia ophthalmo-oto-encephalica. A disorder characterized by amyloid deposition in the walls of the blood vessels of the cerebrum, choroid plexus, cerebellum, spinal cord and retina. Plaques and neurofibrillary tangles are observed in the hippocampus. Clinical features include progressive ataxia, dementia, cataracts and deafness. ADan amyloidogenic peptide variant is cleaved at the normal furin processing site to generate peptide that accumulates in the brain and produces amyloid fibrils responsible for neuronal dysfunction and dementia. Belongs to the ITM2 family. Note: This description may include information from UniProtKB.
Protein type: Membrane protein, integral
Cellular Component: Golgi apparatus; extracellular space; intracellular membrane-bound organelle; extracellular region; plasma membrane; endosome membrane
Molecular Function: protein binding; beta-amyloid binding; ATP binding
Biological Process: nervous system development; negative regulation of amyloid precursor protein biosynthetic process
Reference #:  Q9Y287 (UniProtKB)
Alt. Names/Synonyms: ABRI; ABri/ADan amyloid peptide; BRI; BRI2; BRICD2B; BRICHOS domain containing 2B; E25B; E3-16; FBD; Integral membrane protein 2B; ITM2B; Protein E25B; Transmembrane protein BRI
Gene Symbols: ITM2B
Molecular weight: 30,338 Da
Basal Isoelectric point: Predict pI for various phosphorylation states
Select Structure to View Below

ITM2B

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

 
0 2 K3-u _____MVkVTFNSAL
0 131 K13-u FNSALAQkEAkkDEP
0 24 K16-u ALAQkEAkkDEPkSG
0 20 K17-u LAQkEAkkDEPkSGE
0 9 K21-u EAkkDEPkSGEEALI
0 10 K39-u DAVAVDCkDPDDVVP
  mouse

 
K3-u _____MVkVTFNSAL
K13-u FNSALAQkEAkkDEP
K16-u ALAQkEAkkDEPkSS
K17-u LAQkEAkkDEPkSSE
K21-u EAkkDEPkSSEEALI
K39-u DAVAVDCkDPGDVVP
  rat

 
K3 _____MVKVTFNSAL
K13-u FNSALAQkEAkkDEP
K16-u ALAQkEAkkDEPkSS
K17-u LAQkEAkkDEPkSSE
K21-u EAkkDEPkSSEEALI
K39 DAVAVDCKDPDDVVP
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