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Review
. 2020 Jan 29;69(1):1-10.
doi: 10.1538/expanim.19-0076. Epub 2019 Oct 1.

Role of MafB in macrophages

Michito Hamada  1   2 , Yuki Tsunakawa  1   3 , Hyojung Jeon  1   2 , Manoj Kumar Yadav  1   3 , Satoru Takahashi  1   2
Affiliations
Review

Role of MafB in macrophages

Michito Hamada et al. Exp Anim. .

Abstract

The transcription factor MafB regulates macrophage differentiation. However, studies on the phenotype of Mafb-deficient macrophages are still limited. Recently, it was shown that the specific expression of MafB permits macrophages to be distinguished from dendritic cells. In addition, MafB has been reported to be involved in various diseases related to macrophages. Studies using macrophage-specific Mafb-deficient mice show that MafB is linked to atherosclerosis, autoimmunity, obesity, and ischemic stroke, all of which exhibit macrophage abnormality. Therefore, MafB is hypothesized to be indispensable for the regulation of macrophages to maintain systemic homeostasis and may serve as an innovative target for treating macrophage-related diseases.

Keywords: MafB; homeostasis; large Maf family; macrophage; transcription factor.

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Figures

Fig. 1.
Fig. 1.
Structural features of Maf proteins. A. Schematic diagrams of four large Maf and three small Maf protein structures. Their amino acid lengths are indicated on the right side. The small Maf proteins are essentially composed of a carboxy-terminal basic leucine zipper (b-Zip) domain and a DNA-binding domain, whereas the large Maf proteins contain an additional transactivation domain. B. Maf proteins bind as homodimers to two types of target sequences, the classical Maf recognition element (MARE) site and the 5’-AT-rich MARE half-site.
Fig. 2.
Fig. 2.
Schematic model of the major regulatory factors of MafB induced by an external stimulus. In macrophages, MafB is regulated by food, cell debris, and waste via the regulation of nuclear receptor transcription factors, and it is also controlled by inflammatory signals such as microRNAs or cytokines (left panel). The right table shows macrophage phenotypes and target genes in macrophages involved in several diseases.
Fig. 3.
Fig. 3.
Domain structure and the location of mutations in the human MAFB protein. Each position indicates the amino acid substitution of the observed mutations in patients where mutations were previously reported for multicentric carpotarsal osteolysis (MCTO) and Duane syndrome. The osteolysis disorder MCTO is known to be caused by a dominant missense mutation in the transactivation domain. A mutation in the zinc finger DNA-binding domain of MafB may also cause DRS.
See this image and copyright information in PMC

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