General Information of MIC (ID: MC0512)
  MIC Name
Olsenella profusa F019501
  Lineage Kingdom: Bacteria
Phylum: Actinobacteria
Class: Coriobacteriia
Order: Coriobacteriales
Family: Coriobacteriaceae
Genus: Olsenella
  Oxygen Sensitivity
Obligate anaerobe
  Microbial Metabolism
Saccharolytic; Fermentative
  Gram
Positive
  Host Relationship
Commensal
  Genome Size (bp)
2724935
  Description
Olsenella profusa F0195 is a strain of obligate anaerobic, gram-positive, saccharolytic bacteria.
  External Links Taxonomy ID 1125712
GOLD Database ID Go0012799

Full List of Metabolite(s) Produced by This MIC
     Molecule Type: Choline metabolites
           Metabolite Name: Choline Click to Show/Hide
              Detailed Infomation Meta Info click to show the detail information of this Metabolite
              Metabolic Classification Microbial producted compound [others]
Modification Type Molecule EM Info Cell/Tissue Type Modified sites Condition REF
DNA Methylation SUV39H1 EM Info Liver promoter . [1], [2]
DNA Methylation G9a EM Info Liver promoter . [1], [2]
Histone Dimethylation H3 EM Info Liver lysine 4 . [1], [2]
Histone Dimethylation H3 EM Info Liver lysine 9 . [1], [2]
Histone Dimethylation H3 EM Info Cortex lysine 9 . [3], [1]
Histone Trimethylation H3 EM Info Liver lysine 27 . [1], [2]
Histone Trimethylation H3 EM Info Cortex lysine 27 . [3], [1]
     Molecule Type: Fatty acids
           Metabolite Name: Acetate Click to Show/Hide
              Detailed Infomation Meta Info click to show the detail information of this Metabolite
              Metabolic Classification Microbial producted compound [end-products]
Modification Type Molecule EM Info Cell/Tissue Type Modified sites Condition REF
Histone Acetylation H3K56 EM Info HepG2 cells FASN promoter Hypoxia [4], [1]
Histone Acetylation H3K27 EM Info HepG2 cells FASN promoter Hypoxia [1], [2]
Histone Acetylation H3K27 EM Info HepG2 cells ACACA promoter Hypoxia [3], [1]
Histone Acetylation H3K27 EM Info HepG2 cells LDHA promoter Hypoxia [3], [1]
Histone Acetylation H3K27 EM Info HepG2 cells VEGF promoter Hypoxia [3], [1]
Histone Acetylation H3K56 EM Info HepG2 cells ACACA promoter Hypoxia [3], [1]
Histone Acetylation H3K56 EM Info HepG2 cells LDHA promoter Hypoxia [3], [1]
Histone Acetylation H3K56 EM Info HepG2 cells VEGF promoter Hypoxia [3], [1]
Histone Acetylation H3K9 EM Info HepG2 cells ACACA promoter Hypoxia [3], [1]
Histone Acetylation H3K9 EM Info HepG2 cells FASN promoter Hypoxia [3], [1]
Histone Acetylation H3K9 EM Info HepG2 cells LDHA promoter Hypoxia [3], [1]
Histone Acetylation H3K9 EM Info HepG2 cells VEGF promoter Hypoxia [3], [1]
Histone Deacetylation HDAC9 EM Info Eosinophil cell . Asthma [1], [2]
           Metabolite Name: Lactate Click to Show/Hide
              Detailed Infomation Meta Info click to show the detail information of this Metabolite
              Metabolic Classification Microbial producted compound [end-products]
Modification Type Molecule EM Info Cell/Tissue Type Modified sites Condition REF
miRNA miR-141-3P EM Info Oral epithelial cells . Autistic spectrum disorder [5], [1]


References
1 The Virtual Metabolic Human database: integrating human and gut microbiome metabolism with nutrition and disease. Nucleic Acids Res. 2019 Jan 8;47(D1):D614-D624. doi: 10.1093/nar/gky992.
2 Gestational choline supply regulates methylation of histone H3, expression of histone methyltransferases G9a (Kmt1c) and Suv39h1 (Kmt1a), and DNA methylation of their genes in rat fetal liver and brain. J Biol Chem. 2009 Jan 23;284(4):1982-9. doi: 10.1074/jbc.M807651200. Epub 2008 Nov 10.
3 Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia. Nat Commun. 2016 Jun 30;7:11960. doi: 10.1038/ncomms11960.
4 Evidence that asthma is a developmental origin disease influenced by maternal diet and bacterial metabolites. Nat Commun. 2015 Jun 23;6:7320. doi: 10.1038/ncomms8320.
5 Potential Associations Among Alteration of Salivary miRNAs, Saliva Microbiome Structure, and Cognitive Impairments in Autistic Children. Int J Mol Sci. 2020 Aug 27;21(17):6203. doi: 10.3390/ijms21176203.

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