Ketogenic treatment reduces deleted mitochondrial DNAs in cultured human cells.

Impairment of mitochondrial energy metabolism has been associated with a wide range of human disorders. Large-scale partial deletions of mitochondrial DNA (mtDNA) cause sporadic Kearns-Sayre syndrome, a fatal multisystem disorder, in which the majority of mtDNAs in affected tissues have deletions (Delta-mtDNAs). Since most mtDNA-related diseases, including Kearns-Sayre syndrome, are recessive, only a few wild-type mtDNAs can compensate for the deleterious effects of many Delta-mtDNAs.

An algal nucleus-encoded subunit of mitochondrial ATP synthase rescues a defect in the analogous human mitochondrial-encoded subunit.

Unlike most organisms, the mitochondrial DNA (mtDNA) of Chlamydomonas reinhardtii, a green alga, does not encode subunit 6 of F(0)F(1)-ATP synthase. We hypothesized that C. reinhardtii ATPase 6 is nucleus encoded and identified cDNAs and a single-copy nuclear gene specifying this subunit (CrATP6, with eight exons, four of which encode a mitochondrial targeting signal).

Effect of active and passive immunization of male and female rats with a recombinantly expressed bonnet monkey pituitary GnRH receptor fragment.

Gonadotropin releasing hormone (GnRH) exerts its action by binding to the specific receptor which belongs to the family of G-protein coupled receptors that are characterized by the presence of seven transmembrane domains linked together by extracellular and intracellular loops. A fragment of the pituitary receptor of the bonnet monkey (Macaca radiata) corresponding to amino acids 164-266 was cloned and expressed in Escherichia coli. This was used to raise antibodies to the receptor in rabbits.