1. ¹National Jewish Medical and Research Center, Denver, CO, USA
2. ²College of Life Sciences, Wuhan University, Wuhan, China

Correspondence: Dr H-B Shu, College of Life Sciences, Wuhan University, Wuhan, China. E-mail: shuh@whu.edu.cn

Received 16 June 2005; Revised 10 August 2005; Accepted 10 August 2005; Published online 26 September 2005.

Abstract

AMID is an apoptosis-inducing factor (AIF)-homologous and mitochondria-associated protein that has been implicated in caspase-independent apoptosis. Transcription of human AMID gene is upregulated by p53 and downregulated in tumors in comparison to their matched normal tissues, suggesting the possibility that AMID is involved in the downstream effects of p53. To investigate the physiological functions of AMID, we generated AMID-deficient mice by gene targeting. AMID-deficient mice are viable and fertile, develop normally and lack obvious phenotypic changes compared to wild-type mice up to 1 year old. AMID^-/- mice up to 1 year old have no spontaneous tumors and show similar fibrosarcoma incidence after MCA inoculation compared to wild-type mice. AMID^-/- embryonic fibroblasts exhibit normal proliferation but slightly increased resistance to genotoxin-induced growth arrest. These findings suggest that AMID is not required for normal development and p53-mediated tumor suppression.