Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.3.1 (citrate synthase)
4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of Rickettsia felis, Bartonella henselae and B. clarridgeiae in 209 fleas (Ctenocephalides felis) obtained from domestic cats and dogs in several locations in Malaysia was investigated in this study. Using a polymerase chain reaction specific for the citrate synthase (gltA) and 17-kD antigenic protein (17kD) genes of rickettsiae, we detected R. felis DNA in 6 (2.9%) fleas. For detection of bartonellae, amplification of the heme-binding protein (pap31) and riboflavin synthase (ribC) genes identified B. henselae and B. clarridgeiae DNA in 24 (11.5%) and 40 (19.1%) fleas, respectively. The DNA of B. henselae and B. clarridgeiae was detected in 10 (4.8%) fleas. Two B. henselae genogroups (Marseille and Houston-1) were detected in this study; genogroup Marseille (genotype Fizz) was found more often in the fleas. The findings in this study suggest fleas as potential vectors of rickettsioses and cat-scratch disease in this country.
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PMID:Molecular detection of Rickettsia felis, Bartonella henselae, and B. clarridgeiae in fleas from domestic dogs and cats in Malaysia. 2204 52

The heme molecule is the prosthetic group of many hemeproteins involved in essential physiological processes, such as electron transfer, transport of gases, signal transduction, and gene expression modulation. However, heme is a pro-oxidant molecule capable of propagating reactions leading to the generation of reactive oxygen species. The blood-feeding insect Rhodnius prolixus releases enormous amounts of heme during host blood digestion in the midgut lumen when it is exposed to a physiological oxidative challenge. Additionally, this organism produces a hemolymphatic heme-binding protein (RHBP) that transports heme to pericardial cells for detoxification and to growing oocytes for yolk granules and as a source of heme for embryo development. Here, we show that silencing of RHBP expression in female fat bodies reduced total RHBP circulating in the hemolymph, promoting oxidative damage to hemolymphatic proteins. Moreover, RHBP knockdown did not cause reduction in oviposition but led to the production of heme-depleted eggs (white eggs). A lack of RHBP did not alter oocyte fecundation. However, produced white eggs were nonviable. Embryo development cellularization and vitellin yolk protein degradation, processes that normally occur in early stages of embryogenesis, were compromised in white eggs. Total cytochrome c content, cytochrome c oxidase activity, citrate synthase activity, and oxygen consumption, parameters that indicate mitochondrial function, were significantly reduced in white eggs compared with normal dark red eggs. Our results showed that reduction of heme transport from females to growing oocytes by RHBP leads to embryonic mitochondrial dysfunction and impaired embryogenesis.
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PMID:Silencing of maternal heme-binding protein causes embryonic mitochondrial dysfunction and impairs embryogenesis in the blood sucking insect Rhodnius prolixus. 2398 41