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1 ATP gamma S binding stabilized ClpA and ClpX such that t
2 ATP gamma S plus Ca induced a weak-binding state with mo
3 ATP-gamma-S and 2-methylthio ATP (2-Me-S-ATP) were signi
4 ATP-gamma-S is occluded into the Pgp NBDs at 34 degrees
5 ATP-gamma-S, a poorly hydrolyzable ATP analog, did not s
6 In particular, Mg(2+)GTP gamma S and Mg(2+)ATP gamma S inhibited cyclase activity through a mixed,
8 r presence of the poorly hydrolyzable analog ATP-gamma-S unexpectedly revealed that a large number of
9 nstrate that the nonhydrolyzable ATP analog, ATP gamma S, supports the formation of an isolable leadi
12 nce of ATP or its slowly hydrolyzed analogue ATP-gamma-S, under conditions where a significant fracti
13 d Mn on wild-type and D314E Csk with ATP and ATP gamma S [adenosine 5'-O-(3-thiotriphosphate)] as sub
14 wed either by providing a mixture of ATP and ATP gamma S, a nonphysiological and slowly hydrolyzed AT
15 y active ATP analogs (trinitrophenyl-ATP and ATP gamma S-acetamidoproxyl), to form stable binary comp
21 for 21 days with osteogenic media, ATP, and ATP-gamma-S (a stable agonist of the P2Y receptor) revea
22 helicase protein in the presence of DNA and ATP-gamma-S (1 primase:1 helicase monomer; K(d) approxim
23 -nucleotides including GTP, UTP, AMP-PCP and ATP-gamma-S, but not by PP(i) or AMP, suggesting that ch
24 nder different conditions, using either ATP, ATP gamma S, AMP-PNP or ADP as nucleotide cofactors, we
26 ith the thiophosphate donor analogue of ATP, ATP gamma S, or protein phosphatase 1 and 2A inhibitors
27 weakest bound state of the motor, while ATP, ATP gamma S, AMPPNP, and apyrase all induce a shift towa
29 s nonproductive complex results in rapid ATP/ATP-gamma-S exchange to yield a productive gp45 x gp44/6
34 Although unable to promote binding to DNA, ATP-gamma-S also prevents inactivation of Rad51 at 37 de
37 6) M, dTDP; 3 x 10(-5) M, ATP; 2 x 10(-6) M, ATP gamma S), while binding to the remaining sites is un
40 independent increase in CBF, neither ATP nor ATP- gamma -S induced an increase in CBF when the Ca(2+)
43 treatment of cytosol, as well as addition of ATP gamma S to the chase incubations, led to a stabiliza
45 in with a K(d) = 4 microM in the presence of ATP gamma S at 50 mM KCl, which is 10-20-fold tighter th
51 s of the dependence of this insensitivity on ATP gamma S concentration suggested an apparent dissocia
53 e domain in its apo-state or bound to ADP or ATP-gamma-S show conformations reminiscent of the activa
54 aments formed in the presence of ATP, ADP or ATP-gamma-S showed that efficient Rad51 turnover from ds
58 elded several fragments that differed in the ATP gamma S and ADP-bound forms, and thus revealed confo
60 5-HT and adenosine-5'-O-3-thiotriphosphate (ATP-gamma-S) to acutely isolated ciliated ependymal cell
63 P), and adenosine 5'-O-(3-thiotriphosphate) (ATP-gamma-S) bind with similar affinities to the high-af
64 of ATP, adenosine 5'-O-[3-thiotriphosphate] (ATP gamma S) and alpha,beta methylene adenosine triphosp
65 ce of adenosine 5'-[gamma-thio]triphosphate (ATP[gamma-S]), in a temperature regulated high pressure
67 d the agonist rank potency order ATP = UTP = ATP gamma S > ADP > AMP > > adenosine; adenine, AMP-CPP,
69 ffective in releasing Mge1 from Ssc1 whereas ATP gamma S and AMPPNP could not disrupt the Ssc1/Mge1 c
70 atment with MG132 or replacement of ATP with ATP-gamma-S, a nonhydrolyzable analogue of ATP, suggesti
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