Disease relevance of PRRX2

• This examination suggested that mutations at the PRRX1 and/or PRRX2 loci could result in Nager Acrofacial Dysostosis (NAFD) syndrome [1].
• A new translocation t(9;11)(q34;p15) fuses NUP98 to a novel homeobox partner gene, PRRX2, in a therapy-related acute myeloid leukemia [2].

High impact information on PRRX2

• Important differences in regeneration speed were found, prx2 being the fastest regenerated protein, followed by prx1, whereas prx3 and prx6 were regenerated very slowly [3].
• Thus both HOXB13 and PRX-2 are expressed in patterns consistent with roles in fetal skin development and cutaneous regeneration [4].
• Both genes were predominantly expressed in proliferating fetal fibroblasts and developing dermis, and PRX-2 was downregulated in adult skin [4].
• In a model of scarless fetal skin regeneration, PRX-2 expression was strongly increased compared with unwounded skin and the signal was localized to the wounded dermis, the site of scarless repair [4].
• Two novel human homeobox genes, PRX-2 and HOXB13, were identified that were differentially expressed during fetal versus adult wound healing [4].

Anatomical context of PRRX2

• The activity of the downstream, TATA-like promoter preceded with putative motifs for the homeobox transcription factor PRRX2 is restricted to embryonic fibroblasts and certain cell lines [5].

Associations of PRRX2 with chemical compounds

• Enzymatic deglycosylation with alpha-mannosidase converted PRX1 and PRX2 to immunoreactive products migrating in mobility shift polyacrylamide gels at the positions of PRX2 and PRX3, respectively [6].

Other interactions of PRRX2

• Modulation of the human homeobox genes PRX-2 and HOXB13 in scarless fetal wounds [4].

Analytical, diagnostic and therapeutic context of PRRX2

• The expression pattern of PRRX2 and its close relative, PRRX1, were analyzed in human tissue by RT-PCR [1].

References