Version 5.4
Homo sapiens Gene: CTRB2
Summary
InnateDB Gene IDBG-42422.5
Last Modified 2014-10-13 [Report errors or provide feedback]
Gene Symbol CTRB2
Gene Name chymotrypsinogen B2
Synonyms
Species Homo sapiens
Ensembl Gene ENSG00000168928
Encoded Proteins
IDBP-42424
chymotrypsinogen B2
IDBP-748820
IDBP-750502
IDBP-745719
Protein Structure
Useful resources Stemformatics EHFPI ImmGen
Entrez Gene
Summary Currently no Entrez Summary Available. You might want to check the Summary Sections of the Orthologs.
Gene Information
Type Protein coding
Genomic Location Chromosome 16:75204096-75207185
Strand Reverse strand
Band q23.1
Transcripts
ENST00000303037 ENSP00000303963
ENST00000481611
ENST00000562387 ENSP00000455207
ENST00000567767 ENSP00000457279
ENST00000565656
ENST00000562106 ENSP00000454599
Interactions
Number of Interactions This gene and/or its encoded proteins are associated with 0 experimentally validated interaction(s) in this database.
Gene Ontology

Molecular Function
Accession GO Term
GO:0003824 catalytic activity
GO:0004252 serine-type endopeptidase activity
Biological Process
GO:0006508 proteolysis
GO:0006766 vitamin metabolic process
GO:0006767 water-soluble vitamin metabolic process
GO:0007586 digestion
GO:0009235 cobalamin metabolic process
GO:0022617 extracellular matrix disassembly
GO:0030198 extracellular matrix organization
GO:0044281 small molecule metabolic process
Cellular Component
GO:0005576 extracellular region
GO:0005615 extracellular space
Orthologs
No orthologs found for this gene
Pathways
NETPATH
REACTOME
REACT_118682
Activation of Matrix Metalloproteinases pathway
REACT_169312
Defective HLCS causes multiple carboxylase deficiency pathway
REACT_169313
Defective MUT causes methylmalonic aciduria mut type pathway
REACT_169316
Defective MMAA causes methylmalonic aciduria type cblA pathway
REACT_118779
Extracellular matrix organization pathway
REACT_169120
Defective TCN2 causes hereditary megaloblastic anemia pathway
REACT_11238
Metabolism of water-soluble vitamins and cofactors pathway
REACT_118572
Degradation of the extracellular matrix pathway
REACT_169280
Defective AMN causes hereditary megaloblastic anemia 1 pathway
REACT_169149
Defective MTR causes methylmalonic aciduria and homocystinuria type cblG pathway
REACT_169363
Defective LMBRD1 causes methylmalonic aciduria and homocystinuria type cblF pathway
REACT_169178
Defective CD320 causes methylmalonic aciduria pathway
REACT_169429
Defects in cobalamin (B12) metabolism pathway
REACT_163862
Cobalamin (Cbl, vitamin B12) transport and metabolism pathway
REACT_169169
Defective MMACHC causes methylmalonic aciduria and homocystinuria type cblC pathway
REACT_169238
Defects in biotin (Btn) metabolism pathway
REACT_169403
Defective BTD causes biotidinase deficiency pathway
REACT_169415
Defective GIF causes intrinsic factor deficiency pathway
REACT_169385
Defects in vitamin and cofactor metabolism pathway
REACT_169132
Defective CUBN causes hereditary megaloblastic anemia 1 pathway
REACT_169256
Defective MMADHC causes methylmalonic aciduria and homocystinuria type cblD pathway
REACT_169439
Defective MTRR causes methylmalonic aciduria and homocystinuria type cblE pathway
REACT_111217
Metabolism pathway
REACT_169318
Defective MMAB causes methylmalonic aciduria type cblB pathway
REACT_116125
Disease pathway
REACT_11193
Metabolism of vitamins and cofactors pathway
KEGG
INOH
PID NCI
Cross-References
SwissProt
TrEMBL
UniProt Splice Variant
Entrez Gene
UniGene Hs.610926
RefSeq NM_001025200
HUGO
OMIM
CCDS CCDS32489
HPRD
IMGT
EMBL
GenPept
RNA Seq Atlas

If you use InnateDB for your research, please cite the following publication:

Breuer et al., InnateDB: systems biology of innate immunity and beyond - recent updates and continuing curation. Nucl. Acids Res. (2013) 41 (D1) 

InnateDB is being developed jointly by the Brinkman Laboratory (Simon Fraser University, British Columbia, Canada), the Hancock Laboratory (University of British Columbia, Vancouver, British Columbia) and the Lynn EMBL Australia Group (South Australian Health & Medical Research Institute and Flinders University, Adelaide, Australia).

Funding is currently provided by Allergen and EMBL Australia. Previous funding has been provided by Genome Canada, the Foundation for the National Institutes of Health through the Grand Challenges in Global Health initiative and by Teagasc. InnateDB curated interactions are licensed under the Design Science License. All other data is licensed under the terms of the originating database. Contact: innatedb-mail@sfu.ca