Version 5.4
Bos taurus Gene: FLAD1
Summary
InnateDB Gene IDBG-632363.3
Last Modified 2014-10-13 [Report errors or provide feedback]
Gene Symbol FLAD1
Gene Name FAD synthase
Synonyms
Species Bos taurus
Ensembl Gene ENSBTAG00000000186
Encoded Proteins
IDBP-683968
FAD1 flavin adenine dinucleotide synthetase homolog (S. cerevisiae)Uncharacterized protein
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 ENSG00000160688:
This gene encodes the enzyme that catalyzes adenylation of flavin mononucleotide (FMN) to form flavin adenine dinucleotide (FAD) coenzyme. Alternatively spliced transcript variants encoding distinct isoforms have been observed. [provided by RefSeq, Jul 2008]
Gene Information
Type Protein coding
Genomic Location Chromosome 3:15658831-15664782
Strand Reverse strand
Band
Transcripts
ENSBTAT00000000211 ENSBTAP00000000211
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 11 interaction(s) predicted by orthology.
Predicted by orthology
Total 11 [view]
Gene Ontology

Molecular Function
Accession GO Term
GO:0003824 catalytic activity
GO:0003919 FMN adenylyltransferase activity
Biological Process
GO:0006747 FAD biosynthetic process
GO:0006777 Mo-molybdopterin cofactor biosynthetic process
GO:0008152 metabolic process
Cellular Component
Orthologs
Species
Homo sapiens
Mus musculus
Gene ID
Gene Order
ENSG00000160688
View Gene Order
ENSMUSG00000042642
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
mmu00740
Riboflavin metabolism pathway
INOH
PID NCI
Cross-References
SwissProt
TrEMBL F6R6Q1 Q3ZBF1
UniProt Splice Variant
Entrez Gene 506682
UniGene
RefSeq NM_001035039
HUGO
OMIM
CCDS
HPRD
IMGT
EMBL BC103379 DAAA02007156
GenPept AAI03380
RNA Seq Atlas 506682

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