Senescence-associated beta-galactosidase is lysosomal beta-galactosidase.

By Bo Yun Lee, Jung-A Han, Jun-Sub Im, A. Morrone, K. Johung, E. Goodwin, W. Kleijer, D. DiMaio, E. Hwang. Aging Cell, 2006

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Lamin B1 loss is a senescence-associated biomarker (2012, background): “In addition, the most widely used senescence marker, SA-βgal, is neither necessary nor sufficient for senescence (Dimri et al., 1995; Lee et al., 2006) and is both labile and difficult to detect in vivo.”
Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “These results confirmed that (SA-β-gal) activity is a consequence rather than a cause of the senescent state, and is instead related with the increased lysosomal biogenesis that is observed in these cells (Lee et al., 2006a).”
Therapy-induced senescence in cancer. (2010, background): “Cellular phenotype Morphology† Visual (4,6) SA-b-gal activity Enzyme/staining (12) Glb1 RNA, IHC (86) SSC Flow cytometry (4) Proliferation arrest BrdU Incorporation IHC, flow cytometry (13)”
Four faces of cellular senescence (2011, unknown): “There is mounting evidence that these pathways interact and modulate each other (Zhang et al., 2006; Leong et al., 2009; Su et al., 2009; Yamakoshi et al., 2009).”
DNA damage response and cellular senescence in tissues of aging mice (2009, result): “, 1995), which was not causally related to senescence induction (Lee et al., 2006), was cumbersome at least in some tissues and resulted not too seldom in contradictory data (Kurz et al.”