|Aging Phenotype||Shortened life-span|
|Description||Survival among male animals lacking SMP30 is 50% at 180 days compared to 100% among controls (N. Maruyama, unpublished data).|
|Gene Function||Senescence marker protein-30 (SMP30) is a calcium-binding protein that decreases in an androgen-independent manner with aging and is suggested to protect cells from apoptosis (Ishigami et al., 2002).|
|Other Phenotypes||SMP30-/- mutant mice were indistinguishable from their SMP30+/+ littermates in terms of development and fertilization capability (Ishigami et al., 2002). However, -/- animals were more susceptible to liver injury after treatment with anti-FAS antibody.|
SMP30-/- hepatocytes cultured in vitro were found to be more susceptible to apoptosis induced by tumor necrosis factor-alpha (TNF-alpha) plus actinomycin D (ActD) than SMP30+/+ hepatocytes.
SMP-30 is expressed primarily in the liver where it suppresses cell proliferation (Ishigami et al., 2001) and regulates calcium homeostasis by enhancing plasma membrane calcium ion- pumping activity (Fujita et al., 1999).
|Primary Reference||Ishigami, A., Fujita, T., Handa, S., Shirasawa, T., Koseki, H., Kitamura, T., Enomoto, N., Sato, N., Shimosawa, T., and Maruyama, N. (2002). Senescence marker protein-30 knockout mouse liver is highly susceptible to tumor necrosis factor-alpha- and Fas-me [Abstract]|
|Other References||Ishigami, T., Fujita, T., Simbula, G., Columbano, A., Kikuchi, K., Ishigami, A., Shimosawa, T., Arakawa, Y., and Maruyama, N. (2001). Regulatory effects of senescence marker protein 30 on the proliferation of hepatocytes. Pathol Int 51, 491-7. [Abstract]|
Fujita, T., Shirasawa, T., and Maruyama, N. (1999). Expression and structure of senescence marker protein-30 (SMP30) and its biological significance. Mech Ageing Dev 107, 271-80. [Abstract]
|Relevant Links||LocusLink: http://www.ncbi.nih.gov/LocusLink/LocRpt.cgi?l=19733|
|Keywords||mouse, senescence, biomarker, calcium homeostasis, liver, hepatocytes|