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1 roblasts, HEK293 cells, and murine heart and liver mitochondria.
2 red to as mtMYH, has been purified from calf liver mitochondria.
3 n during 5-HT metabolism in isolated hamster liver mitochondria.
4 selectively localized in highly purified rat liver mitochondria.
5 sely affects the respiratory activity of rat liver mitochondria.
6 roximately 0.5 kD) in the matrix of isolated liver mitochondria.
7 ted to homogeneity from Percoll-purified rat liver mitochondria.
8 nd DA metabolism in isolated hamster and rat liver mitochondria.
9 and blocks mitochondrial pyruvate carrier in liver mitochondria.
10 d to ethanol, far in excess of that in adult liver mitochondria.
11 he permeability transition pore of heart and liver mitochondria.
12 e activity and the MMPT were measured in rat liver mitochondria.
13 s a key participant of ceramide formation in liver mitochondria.
14 findings, based upon their studies of mouse liver mitochondria.
15 e claim that a NOS isoform exists within rat liver mitochondria.
16 ansition (MPT) were assessed in isolated rat liver mitochondria.
17 g proteins derived from HeLa cells and mouse liver mitochondria.
18 pecific, because no decrease was observed in liver mitochondria.
19 ith mastoparan, an inducer of the MPT in rat liver mitochondria.
20 the metabolism of 10-HCO-THF by isolated rat liver mitochondria.
21 er membranes derived from swollen/shrunk rat liver mitochondria.
22 etic acid (DOPAC) in isolated hamster or rat liver mitochondria.
24 s, slightly enhanced respiration in isolated liver mitochondria (30.8% compared with control), lower
26 dicate that increased levels of HNE in fetal liver mitochondria after maternal ethanol consumption re
27 y active state 3 respiration in AdN-depleted liver mitochondria, although further accumulation of AdN
28 nsition (MPT) pore opening in isolated mouse liver mitochondria, an effect that was prevented complet
29 e chose to readdress this question using rat liver mitochondria and employing a variety of assays tha
31 substrates of beta-oxidation in isolated rat liver mitochondria and hence are expected to yield 5,7-d
32 f tetraoleoyl-CL to tetralinoleoyl-CL in rat liver mitochondria and identified the intermediates lino
33 sm and lipid oxidation, is induced in fasted liver mitochondria and implicated in metabolic syndrome.
34 question by measuring K+ flux in intact rat liver mitochondria and in liposomes containing KATP chan
35 rt and oxidative phosphorylation in isolated liver mitochondria and in the cultured murine hepatoma c
36 brain nonsynaptosomal mitochondria and mouse liver mitochondria and mitoplast fractions derived from
37 ltransferase (GPAT) was determined using rat liver mitochondria and mutagenized recombinant rat GPAT
38 t fractionation, ultrapure, never frozen rat liver mitochondria and submitochondrial particles were o
39 atory showed that isolated, intact adult rat liver mitochondria are able to oxidize the 3-carbon of s
42 (MT) localizes in the intermembrane space of liver mitochondria as well as in the cytosol and nucleus
43 r ion trap-mass spectrometry analyses of rat liver mitochondria as well as submitochondrial particles
44 GD3 directly induces the PT in isolated rat liver mitochondria at 30-100 microM in the presence of e
45 re we show that CBS proteins were present in liver mitochondria at a low level under normoxia conditi
46 idated using mouse cortical synaptosomes and liver mitochondria attached to XF24 V7 cell culture micr
51 he mtUDG activity did not change with age in liver mitochondria, but there was a small increase in ac
53 and extent were normal in isolated Mfn2(-/-) liver mitochondria, consistent with the finding that acu
54 s, the P/O ratios obtained with isolated rat liver mitochondria consistently exceed 2.5 with NAD-link
55 l-related decreases in COX activity found in liver mitochondria could be attributable to HNE adduct f
56 he overall activity of the CU in cardiac and liver mitochondria, even at the highest estimated values
62 uding analytical parameters, from a study of liver mitochondria from control and diabetic rats are pr
69 In this study we examined the properties of liver mitochondria from transgenic mice expressing HCV c
74 active proteins in wild type and mtGPAT(-/-) liver mitochondria have different isoelectric points.
76 bited calcium-induced AIF release from mouse liver mitochondria, implicating the involvement of an en
77 y examines the effect of alcohol exposure on liver mitochondria in a rat model and explores the inter
78 responsible for the accumulation of AdNs in liver mitochondria in a strictly Ca(2+)-dependent way wi
79 mitoylcarnitine-supported respiration of rat liver mitochondria in concentration-dependent and time-d
81 ase in oxidative phosphorylation observed in liver mitochondria in response to glucagon and Ca(2+)-mo
86 AdN content, state 3 respiration and CRC in liver mitochondria in wild type but not in SCaMC-3-KO mi
87 istent with this concept, H2O2 production by liver mitochondria increases from 5 minutes to 3 hours a
89 e activity was also observed in isolated rat liver mitochondria incubated with alpha-TOS and tBOOH.
90 expressing HCV core protein, and from normal liver mitochondria incubated with recombinant core prote
92 susceptibility to the calcium-induced MPT in liver mitochondria isolated from a knock-in HD mouse mod
95 antisera against various subfractions of rat liver mitochondria (mitoplast, inner membrane, intermemb
96 Mn-SOD expression and activity of Ad.SOD2 in liver mitochondria of infected animals was increased nea
102 inhibitor of the permeability transition in liver mitochondria, only protects against neuronal injur
103 lity transition or cytochrome c release from liver mitochondria or GCDC-induced mitochondrial depolar
106 ion (109% compared with control) in isolated liver mitochondria, probably due to increased levels of
107 dependent increases in oxidant production by liver mitochondria promote the induction of antioxidant
108 ificantly decreased respiratory rates in rat liver mitochondria relative to untreated controls, compl
110 globin and nitrite to isolated rat heart and liver mitochondria resulted in the inhibition of respira
113 tochondria in PC12 cells and of isolated rat liver mitochondria showed that hypoxia induced depolariz
115 GST release) and NAPQI toxicity in isolated liver mitochondria (succinate dehydrogenase inactivation
118 el of the mPT in populations of isolated rat liver mitochondria that quantitatively describes Ca(2+)-
119 Rottlerin increased the QO2 of isolated rat liver mitochondria to a level similar to that produced w
120 tAPE, we purified the APE activity from beef liver mitochondria to near homogeneity, and showed that
121 were characterized by exposing isolated rat liver mitochondria to physiological and pathological rat
123 ake, even though ruthenium red-inhibited rat liver mitochondria undergo rapid pore opening under anal
126 We found that the GSH content of isolated liver mitochondria was diminished by >/=50% in GGT(-/-)
129 might be linked, respiration of isolated rat liver mitochondria was measured after addition of Zn(2+)
130 se (CPS)-1, a protein primarily localized to liver mitochondria, was found to be present in high conc
131 atory control ratios (RCRs) of GGT(-/-) mice liver mitochondria were </=60% those of wild-type mice p
132 Intact and swelling bovine heart and rat liver mitochondria were examined with an excitation wave
133 nd, recombinant SCAD activity and antigen in liver mitochondria were found up to 7-fold of normal con
134 em mass spectrometry, respectively, when rat liver mitochondria were incubated with elaidoyl-CoA but
135 s end, changes in H(2)O(2) production by rat liver mitochondria were monitored at different rates of
139 ate production was confirmed in isolated rat liver mitochondria where formate production from serine,
140 so be efficiently imported into isolated rat liver mitochondria, where it is processed to its native
141 idation (FAO) proteins were less abundant in liver mitochondria, whereas FAO protein content was indu
142 PHOS subunits were coordinately increased in liver mitochondria, whereas mitochondria of other tissue
143 ificant degradation of mtDNA in isolated rat liver mitochondria, whereas the same concentration of dy
146 mounts of the ROS hydrogen peroxide, whereas liver mitochondria, which express a different Ant isofor
147 heir genomes and isolated a protein from rat liver mitochondria with 8-oxoguanine (8-oxodG) DNA glyco
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