Version 5.4
Bos taurus Gene: ACP5
Summary
InnateDB Gene IDBG-643580.3
Last Modified 2014-10-13 [Report errors or provide feedback]
Gene Symbol ACP5
Gene Name Uncharacterized protein
Synonyms TRAP
Species Bos taurus
Ensembl Gene ENSBTAG00000004826
Encoded Proteins
IDBP-696151
acid phosphatase 5, tartrate resistant
Protein Structure
Useful resources Stemformatics EHFPI ImmGen
Entrez Gene
Summary This gene does not have any Entrez summary - the following is the summary from its human ortholog ENSG00000102575:
This gene encodes an iron containing glycoprotein which catalyzes the conversion of orthophosphoric monoester to alcohol and orthophosphate. It is the most basic of the acid phosphatases and is the only form not inhibited by L(+)-tartrate. [provided by RefSeq, Aug 2008]
Gene Information
Type Protein coding
Genomic Location Chromosome 7:17134691-17137939
Strand Reverse strand
Band
Transcripts
ENSBTAT00000006339 ENSBTAP00000006339
Interactions
Number of Interactions This gene and/or its encoded proteins are associated with 0 experimentally validated interaction(s) in this database.
They are also associated with 8 interaction(s) predicted by orthology.
Predicted by orthology
Total 8 [view]
Gene Ontology

Molecular Function
Accession GO Term
GO:0003993 acid phosphatase activity
GO:0008198 ferrous iron binding
GO:0008199 ferric iron binding
GO:0016787 hydrolase activity
Biological Process
GO:0016311 dephosphorylation
GO:0032496 response to lipopolysaccharide
GO:0032691 negative regulation of interleukin-1 beta production
GO:0032695 negative regulation of interleukin-12 production
GO:0032720 negative regulation of tumor necrosis factor production
GO:0032929 negative regulation of superoxide anion generation
GO:0034097 response to cytokine
GO:0045019 negative regulation of nitric oxide biosynthetic process
GO:0045453 bone resorption
GO:0050728 negative regulation of inflammatory response
GO:0050830 defense response to Gram-positive bacterium
GO:0060349 bone morphogenesis
Cellular Component
GO:0005764 lysosome
GO:0070062 extracellular vesicular exosome
Orthologs
Species
Homo sapiens
Mus musculus
Gene ID
Gene Order
ENSG00000102575
View Gene Order
ENSMUSG00000001348
View Gene Order
Pathway Predictions based on Human Orthology Data
NETPATH
REACTOME
REACT_11070
Vitamin B2 (riboflavin) metabolism 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_169120
Defective TCN2 causes hereditary megaloblastic anemia pathway
REACT_11238
Metabolism of water-soluble vitamins and cofactors 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_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
REACT_189088
Defective LMBRD1 causes methylmalonic aciduria and homocystinuria type cblF pathway
REACT_189085
Disease pathway
REACT_216155
Vitamin B2 (riboflavin) metabolism pathway
REACT_188937
Metabolism pathway
REACT_189089
Defective AMN causes hereditary megaloblastic anemia 1 pathway
REACT_189086
Defective GIF causes intrinsic factor deficiency pathway
REACT_189075
Defective MMAA causes methylmalonic aciduria type cblA pathway
REACT_189076
Defective MMACHC causes methylmalonic aciduria and homocystinuria type cblC pathway
REACT_189078
Defective MMADHC causes methylmalonic aciduria and homocystinuria type cblD pathway
REACT_189098
Defective CD320 causes methylmalonic aciduria pathway
REACT_189097
Defective MUT causes methylmalonic aciduria mut type pathway
REACT_189096
Defects in biotin (Btn) metabolism pathway
REACT_189095
Defective BTD causes biotidinase deficiency pathway
REACT_189093
Defective MMAB causes methylmalonic aciduria type cblB pathway
REACT_189092
Defective MTR causes methylmalonic aciduria and homocystinuria type cblG pathway
REACT_189091
Defective MTRR causes methylmalonic aciduria and homocystinuria type cblE pathway
REACT_189090
Defective CUBN causes hereditary megaloblastic anemia 1 pathway
REACT_254651
Metabolism of vitamins and cofactors pathway
REACT_238663
Metabolism of water-soluble vitamins and cofactors pathway
REACT_189110
Defects in vitamin and cofactor metabolism pathway
REACT_189116
Defects in cobalamin (B12) metabolism pathway
REACT_189114
Defective TCN2 causes hereditary megaloblastic anemia pathway
REACT_189100
Defective HLCS causes multiple carboxylase deficiency pathway
KEGG
hsa00740
Riboflavin metabolism pathway
hsa04142
Lysosome pathway
hsa04380
Osteoclast differentiation pathway
mmu00740
Riboflavin metabolism pathway
mmu04142
Lysosome pathway
mmu04380
Osteoclast differentiation pathway
INOH
PID NCI
Cross-References
SwissProt
TrEMBL E1B8A0 G3M8V1
UniProt Splice Variant
Entrez Gene 517002
UniGene Bt.109701 Bt.5193
RefSeq NM_001256558 XM_005208749
HUGO
OMIM
CCDS
HPRD
IMGT
EMBL DAAA02019487 JN635352
GenPept AEO24285
RNA Seq Atlas 517002

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