1 rkers of cellular senescence, p16(Ink4a) and SA-beta-gal.

2 nated bone marrow progenitor cells expressed SA-beta-gal and senescence-associated proteins p53 and p

3 tosis and senescence, tested as staining for SA-beta-gal, also expressed p16(INK4A).

4 Senescence induction, tested as staining for SA-beta-gal, in reoxygenated progenitor cells was closel

5 h arrest and senescence-associated beta-gal (SA-beta-gal) activity.

6    Senescence-associated beta-galactosidase (SA beta-gal) activity was observed in lymphomas from Emu

7 of senescence-associated beta-galactosidase (SA beta-gal) activity, apparently irreparable genomic DN

8  diameter) anti-PECAM/SA-beta galactosidase (SA-beta-gal) conjugates bound selectively to PECAM-expre

9 of senescence-associated beta-galactosidase (SA-beta-gal) activity [2,3,13-15].

10 ed senescence-associated beta-galactosidase (SA-beta-gal) activity and production of intracellular re

11 nd senescence-associated beta-galactosidase (SA-beta-gal) activity but an increase in adenosine triph

12 xygen species (iROS), SA-beta-galactosidase (SA-beta-gal) activity, and autofluorescence (AF) was ass

13 ested as staining for SA-beta-galactosidase (SA-beta-gal), of bone marrow progenitor cells.

14 ss senescence-associated beta-galactosidase (SA-beta-gal).

15           With age, NSCs exhibited increased SA-beta-gal activity and decreased proliferation and poo

16 conditions and significantly decreased iROS, SA-beta-gal, and AF normally induced by hyperoxic condit

17 ith enhanced expression of senescent markers SA-beta-gal, PML, and p16(INK4a).

18 oreover, inhibition of ATM signaling reduced SA-beta-gal positivity but increased apoptosis of reoxyg