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1 TP channels purified from rat liver and beef heart mitochondria.
2 me profiling, we analyzed the interactome of heart mitochondria.
3 hasome disassembly in WT, but not in CypD KO heart mitochondria.
4 sines 19 and 26 of MPC2 is enhanced in Akita heart mitochondria.
5 ygenases opened the myocardial mPTP in human heart mitochondria.
6 nd energetic substrate availability of mouse heart mitochondria.
7 f complex I purified from Ovis aries (ovine) heart mitochondria.
8 ith experimental data obtained from isolated heart mitochondria.
9 s reinhardtii and cytochrome bc(1) from beef heart mitochondria.
10 brane (85:6:9) distribution of PKA in bovine heart mitochondria.
11  observed only with BM and not with liver or heart mitochondria.
12 tion on ROS production by isolated energized heart mitochondria.
13 h calcium ions (Ca(2+)) signaling in porcine heart mitochondria.
14 f of that of the enzyme purified from bovine heart mitochondria.
15 uced a rapid increase in A520, especially in heart mitochondria.
16 vidence of increased proton leak in the aged heart mitochondria.
17 ctrometric analysis of highly purified human heart mitochondria.
18 tabolite of oleic acid, was studied with rat heart mitochondria.
19 rotein and a cyclophilin D purified from rat heart mitochondria.
20  in Sod2 in heart tissue, and no increase in heart mitochondria.
21  significant decrease from 6 to 23 months in heart mitochondria.
22 e effects of TG on MPT in isolated liver and heart mitochondria.
23            Furthermore, isolated, intact rat heart mitochondria 1) synthesize malonyl-CoA with simult
24               ATP synthesis rates in hypoxic heart mitochondria (3.92+/-0.23 micromol ATP. min(-1). m
25 lationship between complex I from Bos taurus heart mitochondria, a close model for the human enzyme,
26 ution structure of complex I from Bos taurus heart mitochondria, a close relative of the human enzyme
27 R) in newborn Fragile X syndrome (FXS) mouse heart mitochondria, a model system of coenzyme Q excess
28                         We purified from cow heart mitochondria an enzyme (OAT1) with OAA tautomerase
29 tive channel in the native inner membrane of heart mitochondria and characterized its pharmacological
30 ydroxyl radical production in isolated mouse heart mitochondria and F2-isoprostanes in brains and hea
31 ive compounds were tested on isolated murine heart mitochondria and H9c2 cells for their inhibitory a
32                                    In bovine heart mitochondria and in submitochondrial particles, me
33            The precursor was imported by rat heart mitochondria and processed in a single step to a 2
34         We have purified complex I from beef heart mitochondria and reconstituted the enzyme into lip
35 Purified cytochrome b-c1 complexes from beef heart mitochondria and Rhodobacter sphaeroides were reco
36  The cytochrome c oxidase content of porcine heart mitochondria and whole tissue was determined to be
37                     TERT is present in human heart mitochondria, and remote ischemic preconditioning
38 thesis by MF(1), the F(1)-ATPase from bovine heart mitochondria; and (ii) the possibility that the be
39 cattering were evaluated in isolated porcine heart mitochondria at 37 degrees C using a variety of op
40 ty against 48 kD OGDC-E2 when probed on beef heart mitochondria (BHM) but retained reactivity toward
41 e in the rate of pyruvate transport in Akita heart mitochondria but no decrease in the mitochondrial
42 ucture of supercomplex I1III2IV1 from bovine heart mitochondria by cryo-EM at 9 A resolution.
43 structure of intact ATP synthase from bovine heart mitochondria by electron cryomicroscopy of single
44 In contrast to brain mitochondria, liver and heart mitochondria challenged with Ca(2+) experienced su
45 reased the rate of ATP synthesis in normoxic heart mitochondria consistent with mitochondrial K(ATP)
46                   Here, we report that human heart mitochondria contain frataxin species of increasin
47 (NADH:ubiquinone oxidoreductase) from bovine heart mitochondria contains 45 different subunits and ni
48 inhibition of the succinate dehydrogenase in heart mitochondria, contributes to the cause of death in
49                                              Heart mitochondria did not display a substantial alterat
50                 Under conditions of ischemia heart mitochondria expressing MLS-STAT3E exhibited modes
51 155W mutant of Escherichia coli F(1) (bovine heart mitochondria F(1) residue number) can quantitative
52                                     Isolated heart mitochondria from 5-day-old sod2 null animals resp
53                     Analyses of purified rat heart mitochondria from normal and streptozocin-treated
54 xidation of palmitoyl CoA (PCoA) in isolated heart mitochondria from Sham and streptozotocin (STZ)-in
55                                 We have used heart mitochondria from sod2 null mice to better underst
56 e a set of alterations caused by diabetes in heart mitochondria from streptozotocin-treated rats.
57                      Biochemically, isolated heart mitochondria from the highly sensitive 129SVEMS mi
58                                     Isolated heart mitochondria from wild-type (WT) and CypD knockout
59                 Functionally, isolated Akita heart mitochondria have significantly impaired maximal (
60                  Incubation of rat liver and heart mitochondria in KCl medium containing Mg2+ and ino
61 TC and ETC activities in both populations of heart mitochondria in T2DM rats were unchanged.
62 on cryo-EM structure of complex I from mouse heart mitochondria in the closed, active (ready-to-go) r
63 fully demonstrated on preclinical model goat heart mitochondria, in vitro.
64 purified monomeric ATP synthase from porcine heart mitochondria into small unilamellar vesicles (SUVs
65 inone oxidoreductase (complex I) from bovine heart mitochondria is a complicated, energy-transducing,
66 inone oxidoreductase (complex I) from bovine heart mitochondria is a highly complicated, energy trans
67 ce of ryanodine, Ca(2+) uptake into isolated heart mitochondria is suppressed.
68 ur study indicate that metabolic function of heart mitochondria is unchanged in the face of oxidative
69 of OGT and complex IV observed in normal rat heart mitochondria is visibly reduced in diabetic sample
70 ndria as well as unpurified brain, liver and heart mitochondria, isolated from 2- and 10-month-old YA
71 s of studies with CytcO isolated from bovine heart mitochondria, it was suggested that in mitochondri
72                       Parallel activation of heart mitochondria NADH and ATP production by Ca(2+) has
73  With the non-bovine serum albumin brain and heart mitochondria oxidizing succinate, the addition of
74 in, and in native gels of the entire porcine heart mitochondria proteome.
75 9 pmol/mg protein for mouse brain and bovine heart mitochondria, respectively.
76                Peroxidative treatment of rat heart mitochondria results in a gradual increase of the
77 oupling in cardiac muscle using isolated rat heart mitochondria (RHMs).
78 the "OH" state) from several sources (bovine heart mitochondria, Rhodobacter sphaeroides, and Paracoc
79                                Surprisingly, heart mitochondria show a dramatically lower mitochondri
80             Immunoblotting of purified human heart mitochondria showed an intense signal of ERbeta, w
81 experimental data obtained from isolated rat heart mitochondria subjected to physiological conditions
82 spiratory inhibition of MT in liver, but not heart, mitochondria suggest a hitherto unknown biologica
83                                 Isolated rat heart mitochondria supplemented with complex I or II sub
84  Ca(2+) concentrations in isolated brain and heart mitochondria, synaptosomes, fibroblasts, and thymo
85                                   In hypoxic heart mitochondria, the rate of ATP synthesis was not af
86 e evidence of bioenergetic disruption within heart mitochondria, there is little information about th
87 f the rate of ATP hydrolysis by F1 from beef heart mitochondria to the ATP concentration dependence o
88 ochondria as well as resilience of liver and heart mitochondria to the deleterious effect of Ca2+.
89  tyrosine-nitrated proteins generated in the heart mitochondria under different in vitro and in vivo
90 dynamically monitor DeltaPsi of isolated rat heart mitochondria using a ratio fluorescence approach.
91                                              Heart mitochondria utilize multiple Ca(2+) transport mec
92 mitochondrial NAD(P)H generation flux in rat heart mitochondria utilizing pyruvate and malate as subs
93  s.e.m.) and the [Ca2+]m of the injected rat heart mitochondria was 116 +/- 10 nM (n = 18, mean +/- s
94         A high capacity for NO scavenging by heart mitochondria was demonstrated, independent of cyto
95  potential (delta psi(m)) in single isolated heart mitochondria was measured by confocal microscopy w
96 hondrial Ca2+ concentration ([Ca2+]m) in rat heart mitochondria was measured quantitatively by loadin
97 found that membrane depolarization in murine heart mitochondria was sensitized to Ca(2+) by the prese
98 quinone oxidoreductase) purified from bovine heart mitochondria was treated with the detergent N, N-d
99 ld be carried out with as little as 10 ng of heart mitochondria/well and as few as 3 x 10(4) cells/we
100 tional beta-oxidation complex (TOC) from pig heart mitochondria were analyzed with the aim of elucida
101  their interplay with matrix GSH in isolated heart mitochondria were examined.
102 omponents of matrix NADH in isolated porcine heart mitochondria were investigated using time-resolved
103 es (20, 26, and 30 degrees C), revealed that heart mitochondria were less coupled at a lower temperat
104 ings from this study indicate that mahi-mahi heart mitochondria were more temperature sensitive compa
105 re almost completely trimethylated in bovine heart mitochondria, whereas ETFalpha is not methylated.
106 mol/L) and 5-HD (300 micromol/L) in normoxic heart mitochondria, whereas glibenclamide and 5-HD alone
107 on cryo-EM structure of complex I from mouse heart mitochondria with a substrate-like inhibitor, pier
108 on by skeletal muscle, brown fat, brain, and heart mitochondria with an emphasis on conditions under
109             We challenged isolated liver and heart mitochondria with Ca(2+), ROS, and Fe(2+) to induc
110 evious study, we found that treatment of rat heart mitochondria with H(2)O(2) resulted in a decline a
111 the present study, treatment of isolated rat heart mitochondria with H(2)O(2) resulted in a decline a
112       In the present study, treatment of rat heart mitochondria with HNE resulted in the selective in
113 ume, pH(m), and O2 consumption in guinea pig heart mitochondria with or without ruthenium red, carbox
114  to the myocardium, it was hypothesized that heart mitochondria would be more tolerant of temperature

 
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