about
Improved methods for magnetic purification of malaria parasites and haemozoinThe microRNA bantam functions in epithelial cells to regulate scaling growth of dendrite arbors in drosophila sensory neuronsSignificance analysis of lexical bias in microarray dataGenome-wide screen for Salmonella genes required for long-term systemic infection of the mouseSplenic red pulp macrophages produce type I interferons as early sentinels of malaria infection but are dispensable for controlGene expression patterns of dengue virus-infected children from nicaragua reveal a distinct signature of increased metabolism(+)-SJ733, a clinical candidate for malaria that acts through ATP4 to induce rapid host-mediated clearance of Plasmodium.Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation.Microarray-based detection of Salmonella enterica serovar Typhimurium transposon mutants that cannot survive in macrophages and mice.Delineation of diverse macrophage activation programs in response to intracellular parasites and cytokines.The microRNA bantam regulates a developmental transition in epithelial cells that restricts sensory dendrite growth.Krüppel mediates the selective rebalancing of ion channel expression.The Enterococcus faecalis pyr operon is regulated by autogenous transcriptional attenuation at a single site in the 5' leader.Multiple effects of the cellular prion protein on tooth development.Loss of Toll-like receptor 7 alters cytokine production and protects against experimental cerebral malariaModulation of virulence by two acidified nitrite-responsive loci of Salmonella enterica serovar Typhimurium.Delineation of upstream signaling events in the salmonella pathogenicity island 2 transcriptional activation pathway.NK cells and immune "memory"FCRL5 Delineates Functionally Impaired Memory B Cells Associated with Plasmodium falciparum Exposure.The SLC36 transporter Pathetic is required for extreme dendrite growth in Drosophila sensory neurons.Neutrophils prime a long-lived effector macrophage phenotype that mediates accelerated helminth expulsion.Trimming of sequence reads alters RNA-Seq gene expression estimates.A Novel Model of Asymptomatic Plasmodium Parasitemia That Recapitulates Elements of the Human Immune Response to Chronic Infection.Cathelicidin Insufficiency in Patients with Fatal LeptospirosisMacrophage Colony Stimulating Factor Derived from CD4+ T Cells Contributes to Control of a Blood-Borne InfectionEAG2 potassium channel with evolutionarily conserved function as a brain tumor target.Growth phase-dependent response of Helicobacter pylori to iron starvationBrain trauma elicits non-canonical macrophage activation statesToll-like receptor 7 mediates early innate immune responses to malaria.Distinct functional programming of human fetal and adult monocytes.Beyond the transcriptome: completion of act one of the Immunological Genome Project.Molecular definition of the identity and activation of natural killer cells.JUNB is a key transcriptional modulator of macrophage activationVersaCount: customizable manual tally software for cell counting.LuxS is required for persistent pneumococcal carriage and expression of virulence and biosynthesis genes.High-throughput method for detecting genomic-deletion polymorphismsMyeloid expression of the AP-1 transcription factor JUNB modulates outcomes of type 1 and type 2 parasitic infections.Saturated Fatty Acids Engage an IRE1α-Dependent Pathway to Activate the NLRP3 Inflammasome in Myeloid Cells.Traumatic brain injury induces macrophage subsets in the brain.Empirical assessment of the impact of sample number and read depth on RNA-Seq analysis workflow performance
P50
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P50
description
hulumtues
@sq
researcher
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wetenschapper
@nl
հետազոտող
@hy
name
Charles C Kim
@es
Charles C Kim
@nl
Charles C Kim
@sl
Charles C. Kim
@en
type
label
Charles C Kim
@es
Charles C Kim
@nl
Charles C Kim
@sl
Charles C. Kim
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altLabel
Charlie
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prefLabel
Charles C Kim
@es
Charles C Kim
@nl
Charles C Kim
@sl
Charles C. Kim
@en
P106
P1153
35487505600
P21
P31
P496
0000-0001-6474-8227