Abstract
Abstract The mammalian Nit1 gene is homologous to bacterial and plant nitrilases. In the fruit fly D. melanogaster and warms C. elegans, Nit1 is fused to the Fhit gene, whereas in mammals, FHIT and NIT1 are separate genes. FHIT is a tumor suppressor gene located at chromosome region 3p14.2, encompassing the common fragile site of the human genome. Somatic loss of Fhit in humans is associated with cancers in a wide variety of sites, including lung, kidney, stomach, pancreas, cervix, ovary, head and neck, breast, and hematopoetic cells. Proteins that engage in fusion events are expected to jointly participate in a biochemical or cellular pathway and/or to physically interact. Therefore, Nit1 may be functionally related to Fhit. Overexpression of Fhit and Nit1 can induce apoptosis. There was evidence showing that Fhit can induce FADD-mediated cell death. In this study, the in vivo function of Nit1 was analyzed using the Nit1 knockout mice. Various in vitro and in vivo analyses showed that Nit1 plays an important role in regulating cell cycle and proliferation in T lymphocytes.
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