1. ¹Cedars-Sinai Medical Center, Burns & Allen Research Institute, Division of Hematology/Oncology, UCLA School of Medicine, Los Angeles, CA, USA
2. ²Department of Medicine, Kochi Medical School, Kochi, Japan

Correspondence: AM Chumakov, Cedars-Sinai Medical Center, Division of Hematology/Oncology, UCLA School of Medicine, Davis Bldg. 5022, 8700 Beverly Blvd., Los Angeles, CA 90048, USA. E-mail: achumakov@hotmail.com

Received 13 November 2002; Revised 31 July 2003; Accepted 14 August 2003; Published online 5 April 2004.

Abstract

The CCAAT enhancer binding protein epsilon (C/EBP-) transcription factor is expressed predominantly in granulocytes. Mice with a disruption of the C/EBP- gene fail to produce mature granulocytes and eosinophils. Cells derived from the peritoneal exudates of C/EBP- -/- mice lack the expression of a number of chemokines and chemokine receptor genes. We have found a novel C/EBP--dependent promyelocyte-specific gene, mXCP1. mXCP1 belongs to a family of XCP/FIZZ/Resistin genes, which includes four murine genes and two human genes, hXCP1 and hXCP2. These genes have four exons and encode short secreted proteins sharing a ten-cysteine motif. Murine mXCP1, mXCP2 and mXCP3 genes map to murine chromosome 16 and mXCP4 is positioned on chromosome 8; the hXCP1 and hXCP2 genes are located at homologous regions of chromosomes 3 and 19. Introduction of an inducible C/EBP- gene into the NIH3T3 and myeloid cells from C/EBP--null mice line revealed that the conditional expression of C/EBP- induced mXCP1. The HXCP1 gene was identified as a C/EBP--dependent regulatory homologue of mXCP1. The expression data for other members of XCP/FIZZ gene family are presented. Further studies indicate that XCP1 is a secreted protein that is chemotactic to myeloid cells from C/EBP--null mice and is able to interact directly with -defensin.