Articles with the keyword: 
Mitochondrial p32 Is a Critical Mediator of ARF-Induced Apoptosis
kavin submitted, created time 3 months 2 weeks (www.cancercell.org)
The shared exon 2 of the p14ARF-p16INK4a locus is frequently mutated in human cancers. However, in contrast to the exon 1β-encoded N-terminal half of ARF, the function of the exon 2-encoded C-terminal half of ARF has been elusive. The authors report that the mitochondrial protein p32/C1QBP binds the ARF C terminus. They show that p32 is required for ARF to localize to mitochondria and induce apoptosis, and that ARF mutations specifically disrupting p32 binding can impair both of these functions 
Vaccine Injury Case Offers a Clue to the Causes of Autism
jane2007 submitted, created time 5 months 1 week (www.sciam.com)
Could a group of disorders involving the power plants of the cell explain why some vaccinated children develop autism but the vast majority don't?
Mitochondrial Mutations Make Tumors Spread
jane2007 submitted, created time 6 months 2 days (sciencenow.sciencemag.org)
Why is it that cancer often strikes its final, fatal blow when a tumor spreads to other organs? It's because of the metastasis of mitochondrial DNA mutations.
Further review of "three-parent" embryo technique
Darkfrog submitted, created time 7 months 4 weeks (www.nature.com)
This is another discussion of the mother-father-mitochondiadonor embryo that I mentioned the other day. It is significantly more revealing. It seems that the mitochondrial transfer involved moving nuclear DNA from the diseased embryo to the healthy one instead of into an ovum from another source.
It also discusses their methods. It seems that the exchange was performed in embryos that had failed in other experiments. The ten successes came from many failures. The specific success to failure ratio is not given.
"Three-parent" technique: mitochondrial replacement could prevent muscular dystrophy and epilepsy
Darkfrog submitted, created time 8 months 13 hours (news.nationalgeographic.com)
It sounds more impressive than it is -- they've replaced the mitochondria, not portions of the somatic DNA.
A team at Newcastle University has constructed ten embryos, presumably viable, that hold DNA from one man and two women. Doctors see this technique as a means by which parents carrying genetic diseases may have their own (mostly) genetic offspring without going all the way to sperm donors, egg donors or surrogates
How the regulatory protein, IF1, inhibits F1-ATPase from bovine mitochondria
william submitted, created time 1 year 1 week (www.pnas.org)
The structure of bovine F1-ATPase inhibited by a monomeric form of the inhibitor protein, IF1, known as I1–60His, lacking most of the dimerization region, has been determined at 2.1-Ĺ resolution. The resolved region of the inhibitor from residues 8–50 consists of an extended structure from residues 8–13, followed by two -helices from residues 14–18 and residues 21–50 linked by a turn.
Study looks at mitochondrial variation in sperm traits and sperm competitive ability
richard submitted, created time 1 year 2 weeks (www.eurekalert.org)
Study considered an important link in the field of sexual selection, where maternal inheritance of mitochondria may well have its greatest impact on sperm traits and competitive ability but thus far has been largely overlooked.
MedUnion submitted, created time 1 year 3 weeks (www.mupnet.com)
AIM: Natural chemopreventives and antioxidants may modulate the response to chemotherapy. In this study we have examined the chemoadjuvant potential of curcumin and quercetin on cisplatin-mediated cell killing/apoptosis, especially the role of mitochondria in the esophageal cancer cell line Hep-2.
METHODS: Apoptosis was detected by flow cytometry. The protein expression of mitochondrion-related apoptotic mediators, i.e. Bcl-2, Bcl-XL, Bax, cytochrome c, and AIF, were studied by Western Blotting. The transcripts of anti-oxidant enzymes were quantitated by RT-PCR
Mechanism of inhibition of bovine F1-ATPase by resveratrol and related polyphenols
jiangyun submitted, created time 1 year 1 month (www.pnas.org)
The structures of F1-ATPase from bovine heart mitochondria inhibited with the dietary phytopolyphenol, resveratrol, and with the related polyphenols quercetin and piceatannol have been determined at 2.3-, 2.4- and 2.7-Ĺ resolution, respectively. The inhibitors bind to a common site in the inside surface of an annulus made from loops in the three - and three -subunits beneath the "crown" of -strands in their N-terminal domains. This region of F1-ATPase forms a bearing to allow the rotation of the tip of the -subunit inside the annulus during catalysis
merry submitted, created time 1 year 1 month (toxsci.oxfordjournals.org)
"Mn-induced mitochondrial depolarization and ROS production were followed by time- and dose-dependent activation of the apoptotic cell death cascade involving caspase-9 and -3. Notably, DNA fragmentation induced by both Mn treatment and the oxidative stress inducer hydrogen peroxide (100µM) was significantly suppressed in PrPC-cells as compared to PrPKO-cells. Together, these results demonstrate that prion protein interferes with divalent metal Mn uptake and protects against Mn-induced oxidative stress and apoptotic cell death."
Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins
Reviver submitted, created time 1 year 2 months (www.pnas.org)
"Here, researchers have identified a unique role of Bak in mitochondrial fragmentation, a seemingly morphological event that contributes to mitochondrial injury during apoptosis. They show that mitochondrial fragmentation is attenuated in Bak-deficient mouse embryonic fibroblasts, baby mouse kidney cells, and, importantly, also in primary neurons isolated from brain cortex of Bak-deficient mice. In sharp contrast, Bax deficiency does not prevent mitochondrial fragmentation during apoptosis
Leovio submitted, created time 1 year 3 months (ajpcell.physiology.org)
It is a superb review on the structure of the mitochondrial electron transport chain.
Cancer as a “Mitochondriopathy”
MedUnion submitted, created time 1 year 3 months (www.mupnet.com)
Mitochondria are subcellular organelles, whose well-known function is to produce ATP through the oxidative phosphorylation system. Alterations in respiratory activity and mitochondrial DNA (mtDNA) appear to be a general feature of malignant cells. The presence of mtDNA mutations has been reported in various cancer cells, and the abundance of mtDNA damage is consistent with the intrinsic susceptibility to constitutive oxidative stress
addict submitted, created time 1 year 3 months (www.nature.com)
In humans, complex I of the respiratory chain is composed of seven mitochondrial DNA (mtDNA)-encoded and 38 nuclear-encoded subunits that assemble together in a process that is poorly defined. To date, only two complex I assembly factors have been identified and how each functions is not clear. Here, we show that the human complex I assembly factor CIA30 (complex I intermediate associated protein) associates with newly translated mtDNA-encoded complex I subunits at early stages in their assembly before dissociating at a later stage.
collapsar submitted, created time 1 year 3 months (www.pnas.org)
The role of the tumor suppressor retinoblastoma protein (pRb) has been firmly established in the control of cell cycle, apoptosis, and differentiation. Recently, it was demonstrated that lack of pRb promotes a switch from white to brown adipocyte differentiation in vitro. We used the Cre-Lox system to specifically inactivate pRb in adult adipose tissue.
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