exhibit antiapoptotic effects by decreasing calcium ion concentrations, and thus preventing mitochondrial calcium ion overload, depolarization, ATP loss, reactive oxygen species production, cytochrome c release, and ultimately, cell death, overexpression of GHITM produces the opposite effect. Clinical significance GHITM may be involved in tumor metastasis through its interactions with the Bcl-2 family proteins to regulate apoptosis. Its role as an apoptotic regulator may also associate it with innate antiviral responses. Overexpression of GHITM has also been observed to speed up the ageing process in HIV infected patients. Interactions GHITM has been shown to interact with cytochrome c. References Further reading