RNA interference and receptors

@article{blandin_complement-like_2004,

title = {Complement-like protein TEP1 is a determinant of vectorial capacity in the malaria vector Anopheles gambiae},

author = {Stephanie A Blandin and Shin-Hong Shiao and Luis F Moita and Chris J Janse and Andrew P Waters and Fotis C Kafatos and Elena A Levashina},

issn = {0092-8674},

year  = {2004},

date = {2004-01-01},

journal = {Cell},

volume = {116},

number = {5},

pages = {661--670},

abstract = {Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific complement-like protein TEP1 from the mosquito Anopheles gambiae binds to and mediates killing of midgut stages of the rodent malaria parasite Plasmodium berghei. The dsRNA knockdown of TEP1 in adults completely abolishes melanotic refractoriness in a genetically selected refractory strain. Moreover, in susceptible mosquitoes this knockdown increases the number of developing parasites. Our results suggest that the TEP1-dependent parasite killing is followed by a TEP1-independent clearance of dead parasites by lysis and/or melanization. Further elucidation of the molecular mechanisms of TEP1-mediated parasite killing will be of great importance for our understanding of the principles of vectorial capacity in insects.},

keywords = {Animals, Anopheles, blandin, Female, Genetic, Humans, Insect Proteins, Insect Vectors, M3i, Malaria, Models, Molecular, Plasmodium berghei, Polymorphism, Protein Structure, RNA, Sequence Alignment, Tertiary},

pubstate = {published},

tppubtype = {article}

}

@article{,

title = {Microarrays as cancer keys: an array of possibilities},

author = { S. Mohr and G. D. Leikauf and G. Keith and B. H. Rihn},

year  = {2002},

date = {2002-01-01},

journal = {J Clin Oncol},

volume = {20},

number = {14},

pages = {3165-75},

abstract = {Malignant transformation results from accumulation of genetic and epigenetic events. Functional studies of cancer will be crucial to our understanding of its complexity and polymorphism. There is no doubt that emerging genomic and proteomic technologies will facilitate such investigations. Microarray technology is a new and efficient approach to extract data of biomedical relevance for a wide range of applications. In cancer research, it will provide high-throughput and valuable insights into differences in an individual's tumor as compared with constitutional DNA, mRNA expression, and protein expression and activity. Across individuals, comparisons could provide tissue-specific disease signatures that provide diagnosis based on hundreds of informative genes. The resulting product should be a wealth of tumor-associated and tumor-specific biomarkers, which may help in cancer etiology, diagnosis, and therapy and ultimately lead to "molecular nosology" of cancers. This review highlights the recent developments in microarray technologies in cancer research, focuses on the results obtained so far, and describes the eventual use of microarray technology for clinical applications.},

note = {0732-183x 

Journal Article 

Review 

Review, Tutorial},

keywords = {(Genetics), *Gene, *Oligonucleotide, *Sequence, Aberrations, Analysis, Analysis/methods, Animals, Array, Chromosome, DNA/methods, Expression, Genotype, Gov't, Human, Mutation, Neoplasms/*genetics, Neoplastic, Oncogenes/*genetics, P.H.S., Polymorphism, Profiling/methods, Proteome/genetics, Regulation, Sequence, Support, U.S.},

pubstate = {published},

tppubtype = {article}

}