ABCC11

ABCC11 expression is negatively regulated by E(2), but that ABCC11 expression is high in high-expressing ER-alpha breast cancers.

ABCC11 works as tranporters for many drugs, and the expression level of ABCC11 is related with the MDR mechanism. And the SNPs genotype of ABCC11 are also an important determinant of drug resistence sensitivity. So ABCC11 may be one of the biomarkers for the treatment in many cancers.

Usually we use the 5-year overall and relapse-free survival rates. A study shown that a single-nucleotide polymorphism (SNP), i.e. 538G>A (rs17822931), of ABCC11/MRP8, which encodes a 5-FU excretion enzyme was significantly associated with shorter relapse-free survivals. We could use ABCC11/MRP8 polymorphism as biomarker in adjuvant oral chemotherapy with S-1 for non-small cell lung cancer.

ABCC11 has no direct medical use for colon cancer. There was significant correlation with ABCC11 expression and lymph node metastasis, venous invasion and curability. The prognosis in ABCC11 negative cases was poor because of increased cases without curative resection.

There was study revealed significantly reduced expression of ABCC11/MRP8 in gastrointestinal tract cancers compared with other cancers. the ABCC11 mRNA-suppressed NCI-N87 gastric cancer cell line failed to secret pepsinogen I extracellularly.The results indicated a novel function of ABCC11/MRP8 in the regulation of pepsinogen I secretion in the normal gastric chief cells.

Many cell lines could usefule, we used polarized Madin-Darby canine kidney II cells before.

Actually, the SNP (538G>A) of the ABCC11 gene is suggested to be the clinical biomarker. The non-synonymous SNP 538G>A (Gly180Arg) has been found to greatly affect the function and stability of de novo synthesized ABCC11 (Arg180) variant protein. And the genetic polymorphisms of human ABC transporter genes are reportedly related to the risk of certain diseases and patients' responses to medication.

ABCC11 is able to transport a diverse range of lipophilic anions, including cyclic nucleotides, E(2)17betaG, steroid sulfates such as dehydroepiandrosterone (DHEAS) and E(1)S, glutathione conjugates such as leukotriene C4 and dinitrophenyl-S-glutathione, and monoanionic bile acids.

A double recessive ABCC11 can generate a milder odor phenotype, but it's not the only factor that determines body odour. Your native skin microbes, diet and even some medications can alter your body odour and produce a stronger smell, despite your genetic build.

The gene variant is known as ABCC11 and the study authors said that the consistency of earwax is a good indication of those who have it. People who have dry earwax as opposed to sticky earwax are highly likely to have the ABCC11 variant and therefore do not produce under arm body odour.

There are two alleles of ABCC11 that differ by a single nucleotide polymorphism or SNP. While most SNPs don’t change a protein, this one does. The guanine allele is dominant for “wet” earwax and body odor due to sweat; the adenine allele is recessive.To eliminate body odor, you don’t want to turn ABCC11 on but turn it off! And that is a generally hard thing to do. More likely would be to develop a specific inhibitor of ABCC11 - inhibitors of other transporters have been valuable in treating serious disease. But body odor isn’t so serious, and it would be very hard to justify the potential risk involved.

No. Merely, the percentage of the gene is the least in Korean peninsula. There is continuous distribution.

Both ABCC11 538G/G and 538G/A correspond to the wet type, and 538A/A corresponds to the dry type.

The SNP 538G>A in the ABCC11 gene.

The association between the ABCC11 genotype (538G>A) and axillary osmidrosis has enabled us to perform genotyping-based diagnosis of axillary osmidrosis.