ABCC6 expression is regulated by CCAAT/enhancer-binding protein activating a primate-specific sequence located in the first intron of the gene.

Pseudoxanthoma elasticum (PXE), a rare recessive genetic disease causing skin, eye, and cardiovascular lesions, is characterized by the calcification of elastic fibers. The disorder is due to loss-of-function mutations of the ABCC6 gene, but the pathophysiology of the disease is still not understood. Here we investigated the transcriptional regulation of the gene, using DNase I hypersensitivity assay followed by luciferase reporter gene assay.

Application of cellular biosensors for analysis of bioactivity associated with airborne particulate matter.

Exposure to airborne particulate matter (PM) is a known risk factor for adverse health effects observed in many environmental and occupational settings. The pathological mechanisms involved in PM-mediated toxicity depend on the size and contents of particles that vary depending on the source of emission. Chemical compositions of PM show multiple components with different bioavailabilities that are capable of acting on multiple molecular and cellular targets, making it difficult to predict PM-associated toxicity based solely on chemical analysis.

Mithramycin A suppresses expression of the human melanoma-associated gene ABCB8.

The role of the ABCB8 gene in human cells is poorly understood, although it has been suggested to be involved in multidrug resistance in some types of cancers (e.g., melanomas).

The ERK1/2-hepatocyte nuclear factor 4alpha axis regulates human ABCC6 gene expression in hepatocytes.

ABCC6 mutations are responsible for the development of pseudoxanthoma elasticum, a rare recessive disease characterized by calcification of elastic fibers. Although ABCC6 is mainly expressed in the liver the disease has dermatologic, ocular, and cardiovascular symptoms. We investigated the transcriptional regulation of the gene and observed that hepatocyte growth factor (HGF) inhibits its expression in HepG2 cells via the activation of ERK1/2.