Version 5.4
Mus musculus Gene: Pank3
Summary
InnateDB Gene IDBG-162655.6
Last Modified 2014-10-13 [Report errors or provide feedback]
Gene Symbol Pank3
Gene Name pantothenate kinase 3
Synonyms
Species Mus musculus
Ensembl Gene ENSMUSG00000018846
Encoded Proteins
IDBP-162659
pantothenate kinase 3
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 ENSG00000120137:
This gene encodes a protein belonging to the pantothenate kinase family. Pantothenate kinase is a key regulatory enzyme in the biosynthesis of coenzyme A (CoA) in bacteria and mammalian cells. It catalyzes the first committed step in the universal biosynthetic pathway leading to CoA and is itself subject to regulation through feedback inhibition by CoA. This family member is expressed most abundantly in the liver. [provided by RefSeq, Jul 2008]
Gene Information
Type Protein coding
Genomic Location Chromosome 11:35769484-35791285
Strand Forward strand
Band A4
Transcripts
ENSMUST00000018990 ENSMUSP00000018990
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 1 interaction(s) predicted by orthology.
Predicted by orthology
Total 1 [view]
Gene Ontology

Molecular Function
Accession GO Term
GO:0004594 pantothenate kinase activity
GO:0005524 ATP binding
Biological Process
GO:0015937 coenzyme A biosynthetic process
GO:0016310 phosphorylation
Cellular Component
GO:0005737 cytoplasm
Orthologs
Species
Homo sapiens
Bos taurus
Gene ID
Gene Order
ENSG00000120137
View Gene Order
ENSBTAG00000011895
Not yet available
Pathways
NETPATH
REACTOME
KEGG
mmu00770
Pantothenate and CoA biosynthesis pathway
INOH
PID NCI
Pathway Predictions based on Human Orthology Data
NETPATH
REACTOME
REACT_11218
Coenzyme A biosynthesis pathway
REACT_11172
Vitamin B5 (pantothenate) 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
KEGG
hsa00770
Pantothenate and CoA biosynthesis pathway
INOH
PID NCI
Cross-References
SwissProt
TrEMBL
UniProt Splice Variant
Entrez Gene
UniGene Mm.255044 Mm.402763 Mm.474774
RefSeq NM_145962
OMIM
CCDS CCDS24543
HPRD
IMGT
MGI ID
MGI Symbol
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