Alternative titles; symbols
HGNC Approved Gene Symbol: ZFP37
Cytogenetic location: 9q32 Genomic coordinates (GRCh38): 9:113,038,377-113,056,724 (from NCBI)
To identify putative transcription factors involved in chondrocyte differentiation during human endochondral bone formation, Dreyer et al. (1998) screened a human fetal cartilage-specific cDNA library with a degenerate oligonucleotide probe corresponding to a conserved stretch of 8 amino acids from the zinc finger region of the Drosophila Kruppel gene family of DNA-binding proteins. Using this strategy, they identified a novel zinc finger gene, termed ZFP37, which corresponds to a putative transcription factor containing 12 tandemly repeated zinc finger motifs and a Kruppel-associated box (KRAB) domain. The KRAB domain appears to function as a transcriptional repressor and is located in the amino terminus, while the zinc finger repeats are positioned at the carboxy terminus of ZFP37. The gene is expressed at low level as a 3.2-kb mRNA in several tissues, including fetal human cartilage. Sequence comparison demonstrated homology to the mouse Zfp37 gene.
By analysis of a somatic cell hybrid panel and fluorescence in situ hybridization, Dreyer et al. (1998) mapped the ZFP37 gene to chromosome 9q32. The Zfp37 gene in mouse maps to chromosome 4 in a region of syntenic homology to human 9q32. Based on the map location and expression pattern of ZFP37, Dreyer et al. (1998) proposed it as a candidate gene for the Nager type of acrofacial dysostosis (154400) (Zori et al., 1993).
Dreyer, S. D., Zhou, L., Machado, M. A., Horton, W. A., Zabel, B., Winterpacht, A., Lee, B. Cloning, characterization, and chromosomal assignment of the human ortholog of murine Zfp-37, a candidate gene for Nager syndrome. Mammalian Genome 9: 458-462, 1998. [PubMed: 9585434] [Full Text: https://doi.org/10.1007/s003359900796]
Zori, R. T., Gray, B. A., Bent-Williams, A., Driscoll, D. J., Williams, C. A., Zackowski, J. L. Preaxial acrofacial dysostosis (Nager syndrome) associated with an inherited and apparently balanced X;9 translocation: prenatal and postnatal late replication studies. Am. J. Med. Genet. 46: 379-383, 1993. [PubMed: 8357008] [Full Text: https://doi.org/10.1002/ajmg.1320460407]