High impact information on Pias2

• Our data show that regulation of cell adhesion is a major function of the Myc-Miz1 complex and suggest that it may contribute to Myc-induced exit from the epidermal stem cell compartment [1].
• Myc regulates keratinocyte adhesion and differentiation via complex formation with Miz1 [1].
• PIASxbeta acts as an activator of Hoxb1 and is antagonized by Krox20 during hindbrain segmentation [2].
• In this study, we have identified PIASxbeta as a novel direct interactor of Krox20 [2].
• Miz1 is required for early embryonic development during gastrulation [3].

Biological context of Pias2

• A consensus Sp1-binding site or GC box is also necessary for Miz-1-dependent transactivation, but not repression [4].
• These results provide a description of sites that modulate the activity of the initiator-binding protein Miz-1 and indicate a stimulatory role for GC box-binding factors in macrophages and a inhibitory role for E box elements in proliferating cells [4].
• We show that Miz1, which mediates Myc repression of gene expression, is expressed in the epidermal basal layer [1].
• Miz1 is a member of the POZ domain/zinc finger transcription factor family [3].
• Myc represses transcription through Miz1 binding sites [3].

Physical interactions of Pias2

• Repression via c-Myc occurs at the initiator elements, whereas a c-Myc-interacting protein (Miz-1) stimulates transcription [4].

Regulatory relationships of Pias2

• c-Myc represses and Miz-1 activates the murine natural resistance-associated protein 1 promoter [5].

Other interactions of Pias2

• Characterization of the murine Nramp1 promoter: requirements for transactivation by Miz-1 [4].

References