Detail Information of Microbiota Influence

General Information of Drug Transporter (DT)
DT ID DTD0015 Transporter Info
Gene Name ABCC4
Transporter Name Multidrug resistance-associated protein 4
Gene ID
10257
UniProt ID
O15439
Microbiota Influence of This DT (MBI)

Bacteria: Pseudomonadota

   Genus: Escherichia

     Escherichia coli 

Microbe Info

Click to Show/Hide the Full List 1 Microbe Influence Related to This Species      

       Microbe Influence1

 Sequestration of human ABCC4 substrates/drugs in the health condition [1]

Detailed Description

 The Escherichia coli str. K-12 substr. MG1655 has been reported to sequester the drug Ciprofloxacin, which limits the distribution of the drug in the body and its binding to the drug transporter ABCC4, thereby affecting the efficacy, safety, or bioavailability of the drug.

Bacteria: Host unspecified microbiota

   Genus: Unknown microbiota

     Host unspecified microbiota 

Click to Show/Hide the Full List 9 Microbe Influence Related to This Species      

       Microbe Influence1

 Down regulating of ABCC4 expression in clostridium difficile infection condition [2]

Regulating Factor
urolithin A

Studied Phenotype

 Colitis [ICD11: 1A40.0]

In Vitro Model

 HT29 cells

Detailed Description

 The metabolite urolithin A generated from the metabolism of dietary precursors by the host unspecified microbiota has been reported to downregulate the expression of the drug transporter ABCC4.

       Microbe Influence2

 Inhibition of ABCC4 function in chronic kidney disease condition [3], [4]

Regulating Factor
p-Cresol glucuronide

Studied Phenotype

 Chronic kidney disease [ICD11: GB61]

Studied Tissue

 Kidney

In Vitro Model

 Human renal proximal tubule cells

Detailed Description

 The metabolite p-cresol glucuronide generated from the metabolism of p-cresol by the host unspecified microbiota has been reported to inhibit the function of the drug transporter ABCC4.

       Microbe Influence3

 Inhibition of ABCC4 function in chronic kidney disease condition [3], [4]

Regulating Factor
p-Cresol sulfate

Studied Phenotype

 Chronic kidney disease [ICD11: GB61]

Studied Tissue

 Kidney

In Vitro Model

 Human renal proximal tubule cells

Detailed Description

 The metabolite p-cresol sulfate generated from the metabolism of p-cresol by the host unspecified microbiota has been reported to inhibit the function of the drug transporter ABCC4.

       Microbe Influence4

 Up regulating of ABCC4 expression in the health condition [5]

Regulating Factor
Bile acid (Chenodeoxycholic acid)

Regulation Mechanism

 via enhancement of Nuclear receptor subfamily 1 group I member 2 (NR1I2) Transcription Factor Info

Studied Tissue

 Liver

Detailed Description

 The metabolite bile acid (chenodeoxycholic acid) generated from the host unspecified microbiota has been reported to increase the expression of the drug transporter ABCC4.

       Microbe Influence5

 Up regulating of ABCC4 expression in the health condition [5]

Regulating Factor
Bile acid (Cholic acid)

Regulation Mechanism

 via enhancement of Nuclear receptor subfamily 1 group I member 2 (NR1I2) Transcription Factor Info

Studied Tissue

 Liver

Detailed Description

 The metabolite bile acid (cholic acid) generated from the host unspecified microbiota has been reported to increase the expression of the drug transporter ABCC4.

       Microbe Influence6

 Up regulating of ABCC4 expression in the health condition [5]

Regulating Factor
Bile acid (Deoxycholic acid)

Regulation Mechanism

 via enhancement of Nuclear receptor subfamily 1 group I member 2 (NR1I2) Transcription Factor Info

Studied Tissue

 Liver

Detailed Description

 The metabolite bile acid (deoxycholic acid) generated from the host unspecified microbiota has been reported to increase the expression of the drug transporter ABCC4.

       Microbe Influence7

 Up regulating of ABCC4 expression in the health condition [5]

Regulating Factor
Bile acid (Hyodeoxycholic acid)

Regulation Mechanism

 via enhancement of Nuclear receptor subfamily 1 group I member 2 (NR1I2) Transcription Factor Info

Studied Tissue

 Liver

Detailed Description

 The metabolite bile acid (hyodeoxycholic acid) generated from the host unspecified microbiota has been reported to increase the expression of the drug transporter ABCC4.

       Microbe Influence8

 Up regulating of ABCC4 expression in the health condition [5]

Regulating Factor
Bile acid (Lithocholic acid)

Regulation Mechanism

 via enhancement of Nuclear receptor subfamily 1 group I member 2 (NR1I2) Transcription Factor Info

Studied Tissue

 Liver

Detailed Description

 The metabolite bile acid (lithocholic acid) generated from the host unspecified microbiota has been reported to increase the expression of the drug transporter ABCC4.

       Microbe Influence9

 Up regulating of ABCC4 expression in hyperuricaemia condition [6]

Studied Phenotype

 Hyperuricaemia [ICD11: 5C55.Y]

Studied Tissue

 Kidney

In Vivo Model

 ICR specific-pathogen-free mice

Detailed Description

 The host unspecified microbiota has been reported to increase the expression of the drug transporter ABCC4.
References
1 Predictive compound accumulation rules yield a broad-spectrum antibiotic. Nature. 2017 May 18;545(7654):299-304.
2 Enhancement of the gut barrier integrity by a microbial metabolite through the Nrf2 pathway. Nat Commun. 2019 Jan 9;10(1):89.
3 Impact of Altered Intestinal Microbiota on Chronic Kidney Disease Progression. Toxins (Basel). 2018 Jul 19;10(7):300.
4 Proximal tubular efflux transporters involved in renal excretion of p-cresyl sulfate and p-cresyl glucuronide: Implications for chronic kidney disease pathophysiology. Toxicol In Vitro. 2015 Oct;29(7):1868-77.
5 Bile acid metabolism and signaling, the microbiota, and metabolic disease. Pharmacol Ther. 2022 Sep;237:108238.
6 The gut microbiota mediates the protective effects of anserine supplementation on hyperuricaemia and associated renal inflammation. Food Funct. 2021 Oct 4;12(19):9030-9042.

If you find any error in data or bug in web service, please kindly report it to Dr. Li and Dr. Fu.