Disease relevance of cytb

• A fragment of the mitochondrial cytochrome b gene of avian malaria (genera Haemoproteus and Plasmodium) was amplified from blood samples of 12 species of passerine birds from the genera Acrocephalus, Phylloscopus and Parus [1].

High impact information on cytb

• In the accompanying paper (S. M. Aldritt, J. T. Joseph, and D. F. Wirth, Mol. Cell. Biol. 9:3614-3620, 1989), evidence is presented that element contains the mitochondrial genes for the protein cytochrome b and a fragment of the large rRNA [2].
• To better understand the molecular basis of atovaquone resistance, we have introduced seven of the mutations from atovaquone-resistant P. jirovecii into the cytochrome b gene of Saccharomyces cerevisiae and thus obtained cytochrome bc(1) complexes resistant to inhibition by atovaquone [3].
• A combined treatment of T. gondii-infected cells with HDQ and the antimalarial agent atovaquone, which blocks the ubiquinol oxidation site of cytochrome b in complex III, resulted in synergism, with a calculated fractional inhibitory concentration of 0.16 nM [4].
• Eight cytb polymorphisms were found outside the ubiquinone reduction site by sequencing the entire gene of 270 isolates [5].
• Atovaquone susceptibility was determined using an in vitro isotopic test and cytb genotyping was performed by restriction fragment length polymorphism analysis and sequencing [5].

Biological context of cytb

• RESULTS: No in vitro atovaquone resistance (IC50 > 1900 nM) and no cytb mutation leading to the Y268S substitution were detected among 477 unexposed African P. falciparum isolates [5].
• We determined the nucleotide sequence of the Babesia gibsoni cytochrome b (cytb) gene [6].
• These results indicate that single nucleotide polymorphisms in the sequence for mitochondrial cytb gene may be associated with decreased susceptibility of Babesia species to atovaquone [6].
• DNA was extracted from B. gibsoni isolated from Aomori Prefecture, Japan, and 1,288 basepairs of the cytb gene, including 1,071 basepairs of the open reading frame, were sequenced [6].
• No known point mutations in cytochrome b gene (cytb), associated with atovaquone resistance, were detected in any recrudescing parasites [7].

Associations of cytb with chemical compounds

• OBJECTIVES: We examined the atovaquone in vitro susceptibility and the cytochrome b (cytb) gene polymorphism of African Plasmodium falciparum isolates during the first years of atovaquone/proguanil use [5].
• Additionally, we investigated the parasite cytochrome b gene of a patient returning from Mali with Malarone treatment failure in vivo [8].
• METHODS: Cultures were sequentially subjected to increasing doses of atovaquone alone or in combination with cycloguanil and the cytochrome b gene was sequenced [8].
• The nucleotide sequences of cytochrome b gene at Qi/quinone binding site from both stages were analyzed using thermal cycle sequencing and were found to be the same [9].
• BACKGROUND: In vitro and in vivo resistance of Plasmodium falciparum to atovaquone or atovaquone-proguanil hydrochloride combination has been associated to two point mutations in the parasite cytochrome b (cytb) gene (Tyr268Ser and Tyr268Asn) [10].

Analytical, diagnostic and therapeutic context of cytb

• Polymerase chain reaction and sequence analysis of the primary and recrudescent isolates confirmed the acquisition of a point mutation (Tyr268Ser) in the cytochrome b gene of the recrudescent isolate known to confer high-level resistance to atovaquone [11].
• Nested cytochrome b polymerase chain reaction diagnostics underestimate mixed infections of avian blood haemosporidian parasites: microscopy is still essential [12].
• Plasmodium falciparum resistance to atovaquone-proguanil has so far been associated with Y268S or Y268N mutations in cytochrome b, although these changes were identified in only seven of the 11 treatment failures [13].

References