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Protein Page:
calreticulin 3 (human)
p Phosphorylation
ac Acetylation
me Methylation
m1 Mono-methylation
m2 Di-methylation
m3 Tri-methylation
ub Ubiquitination
sm Sumoylation
ne Neddylation
gl O-GlcNAc
ga O-GalNAc
pa Palmitoylation
ad Adenylylation
sn S-Nitrosylation
ca Caspase cleavage
sc Succinylation

Overview
calreticulin 3 During spermatogenesis, may act as a lectin-independent chaperone for specific client proteins such as ADAM3. Required for sperm fertility. CALR3 capacity for calcium- binding may be absent or much lower than that of CALR. Defects in CALR3 are the cause of familial hypertrophic cardiomyopathy type 19 (CMH19). CMH19 is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death. Belongs to the calreticulin family. Note: This description may include information from UniProtKB.
Protein type: Cancer Testis Antigen (CTA); Chaperone
Cellular Component: endoplasmic reticulum lumen
Molecular Function: unfolded protein binding; calcium ion binding
Biological Process: protein folding; spermatogenesis; cell differentiation
Reference #:  Q96L12 (UniProtKB)
Alt. Names/Synonyms: CALR3; calreticulin 2; calreticulin 3; Calreticulin-2; Calreticulin-3; cancer/testis antigen 93; CRT2; CT93; FLJ25355; MGC26577
Gene Symbols: CALR3
Molecular weight: 44,996 Da
Basal Isoelectric point: 6.19  Predict pI for various phosphorylation states
Select Structure to View Below

calreticulin 3

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 1 Y57-p RLSSGKFyGHKEKDK
0 1 K89-ac KPFSNKGkTLVIQYT
0 1 T209-p LTSLKKEtsPAEsKD
0 1 S210-p TSLKKEtsPAEsKDW
0 1 S214-p KEtsPAEsKDWEQTK
0 1 K230-ac NKAQDWEkHFLDAST
0 1 S309 LELWQVRSGTIFDNF
0 1 T311 LWQVRSGTIFDNFLI
0 1 Y374-p KINRHEHyFNQFHRR
  mouse

 
Y57 RVSSGKFYGHKEKDK
K89 KPFSNKGKTLVIQYT
K210 TSLRKTEKTSLDSRD
T211 SLRKTEKTSLDSRDW
S215 TEKTSLDSRDWDQVE
K231 SKVQDWEKHFLDAGA
S306-p LELWQVRsGtIFDNF
T308-p LWQVRsGtIFDNFLI
- gap
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