<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Brenton AA</submitter><funding>NIAID NIH HHS</funding><pagination>287</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4077580</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Susceptibility to Plasmodium infection in Anopheles gambiae has been proposed to result from naturally occurring polymorphisms that alter the strength of endogenous innate defenses. Despite the fact that some of these mutations are known to introduce non-synonymous substitutions in coding sequences, these mutations have largely been used to rationalize knockdown of associated target proteins to query the effects on parasite development in the mosquito host. Here, we assay the effects of engineered mutations on an immune signaling protein target that is known to control parasite sporogonic development. By this proof-of-principle work, we have established that naturally occurring mutations can be queried for their effects on mosquito protein function and on parasite develo</pubmed_abstract><journal>Parasites &amp; vectors</journal><pubmed_title>Engineered single nucleotide polymorphisms in the mosquito MEK docking site alter Plasmodium berghei development in Anopheles gambiae.</pubmed_title><pmcid>PMC4077580</pmcid><funding_grant_id>R01 AI078183</funding_grant_id><funding_grant_id>T32 AI074550</funding_grant_id><funding_grant_id>R01 AI080799</funding_grant_id><funding_grant_id>R01AI080799</funding_grant_id><pubmed_authors>Brault AC</pubmed_authors><pubmed_authors>Souvannaseng L</pubmed_authors><pubmed_authors>Anishchenko M</pubmed_authors><pubmed_authors>Luckhart S</pubmed_authors><pubmed_authors>Brenton AA</pubmed_authors><pubmed_authors>Cheung K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Engineered single nucleotide polymorphisms in the mosquito MEK docking site alter Plasmodium berghei development in Anopheles gambiae.</name><description>&lt;h4>Background&lt;/h4>Susceptibility to Plasmodium infection in Anopheles gambiae has been proposed to result from naturally occurring polymorphisms that alter the strength of endogenous innate defenses. Despite the fact that some of these mutations are known to introduce non-synonymous substitutions in coding sequences, these mutations have largely been used to rationalize knockdown of associated target proteins to query the effects on parasite development in the mosquito host. Here, we assay the effects of engineered mutations on an immune signaling protein target that is known to control parasite sporogonic development. By this proof-of-principle work, we have established that naturally occurring mutations can be queried for their effects on mosquito protein function and on parasite develo</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jun</publication><modification>2025-04-18T15:05:38.157Z</modification><creation>2019-03-27T01:31:13Z</creation></dates><accession>S-EPMC4077580</accession><cross_references><pubmed>24957684</pubmed><doi>10.1186/1756-3305-7-287</doi></cross_references></HashMap>