Nelson V. Simwela
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View article: Incorporation of macrophage immune stresses into an intracellular assay of drug tolerance in <i>Mycobacterium tuberculosis</i>
Incorporation of macrophage immune stresses into an intracellular assay of drug tolerance in <i>Mycobacterium tuberculosis</i> Open
Development of new and improved tuberculosis (TB) chemotherapies is hampered by antibiotic resistance and drug tolerance by Mycobacterium tuberculosis ( Mtb ). Phenotypic drug tolerance, a phenomenon where Mtb populations can temporarily s…
View article: Incorporation of macrophage immune stresses into an assay for drug tolerance in intracellular <i>Mycobacterium tuberculosis</i>
Incorporation of macrophage immune stresses into an assay for drug tolerance in intracellular <i>Mycobacterium tuberculosis</i> Open
Development of new and improved tuberculosis (TB) chemotherapies is hampered by antibiotic resistance and drug tolerance by Mycobacterium tuberculosis ( Mtb ). Phenotypic drug tolerance, a phenomenon where Mtb populations can temporarily s…
View article: Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of Mycobacterium tuberculosis
Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of Mycobacterium tuberculosis Open
Mycobacterium tuberculosis ( Mtb ) infection of macrophages reprograms cellular metabolism to promote lipid retention. While it is clearly known that intracellular Mtb utilize host-derived lipids to maintain infection, the role of macropha…
View article: Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of Mycobacterium tuberculosis
Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of Mycobacterium tuberculosis Open
Mycobacterium tuberculosis (Mtb) infection of macrophages reprograms cellular metabolism to promote lipid retention. While it is clearly known that intracellular Mtb utilize host derived lipids to maintain infection, the role of macrophage…
View article: Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of Mycobacterium tuberculosis
Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of Mycobacterium tuberculosis Open
Mycobacterium tuberculosis (Mtb) infection of macrophages reprograms cellular metabolism to promote lipid retention. While it is clearly known that intracellular Mtb utilize host derived lipids to maintain infection, the role of macrophage…
View article: Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of Mycobacterium tuberculosis
Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of Mycobacterium tuberculosis Open
Mycobacterium tuberculosis ( Mtb ) infection of macrophages reprograms cellular metabolism to promote lipid retention. While it is clearly known that intracellular Mtb utilize host-derived lipids to maintain infection, the role of macropha…
View article: Genome-wide screen of Mycobacterium tuberculosis-infected macrophages revealed GID/CTLH complex-mediated modulation of bacterial growth
Genome-wide screen of Mycobacterium tuberculosis-infected macrophages revealed GID/CTLH complex-mediated modulation of bacterial growth Open
The eukaryotic Glucose Induced Degradation/C-Terminal to LisH (GID/CTLH) complex is a highly conserved E3 ubiquitin ligase involved in a broad range of biological processes. However, a role of this complex in host anti-microbial defenses h…
View article: Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of <i>Mycobacterium tuberculosis</i>
Impaired fatty acid import or catabolism in macrophages restricts intracellular growth of <i>Mycobacterium tuberculosis</i> Open
Mycobacterium tuberculosis ( Mtb ) infection of macrophages reprograms cellular metabolism to promote lipid retention. While it is clearly known that intracellular Mtb utilize host derived lipids to maintain infection, the role of macropha…
View article: Genome-wide screen of<i>Mycobacterium tuberculosis-</i>infected macrophages identified the GID/CTLH complex as a determinant of intracellular bacterial growth
Genome-wide screen of<i>Mycobacterium tuberculosis-</i>infected macrophages identified the GID/CTLH complex as a determinant of intracellular bacterial growth Open
Summary The eukaryotic GID/CTLH complex is a highly conserved E3 ubiquitin ligase involved in a broad range of biological processes. However, a role of this complex in host antimicrobial defenses has not been described. We exploited Mycoba…
View article: A conserved metabolic signature associated with response to fast-acting anti-malarial agents
A conserved metabolic signature associated with response to fast-acting anti-malarial agents Open
Characterizing the mode of action of anti-malarial compounds that emerge from high-throughput phenotypic screens is central to understanding how parasite resistance to these drugs can emerge. Here, we have employed untargeted metabolomics …
View article: A conserved metabolic signature associated with response to fast-acting antimalarial agents
A conserved metabolic signature associated with response to fast-acting antimalarial agents Open
Characterizing the mode of action of antimalarial compounds that emerge from high-throughput phenotypic screens is central to understanding how parasite resistance to these drugs can emerge. Here, we have employed untargeted metabolomics t…
View article: Plasmodium berghei K13 Mutations Mediate <i>In Vivo</i> Artemisinin Resistance That Is Reversed by Proteasome Inhibition
Plasmodium berghei K13 Mutations Mediate <i>In Vivo</i> Artemisinin Resistance That Is Reversed by Proteasome Inhibition Open
Recent successes in malaria control have been seriously threatened by the emergence of Plasmodium falciparum parasite resistance to the frontline artemisinin drugs in Southeast Asia. P. falciparum artemisinin resistance is associated with …
View article: <i>Plasmodium berghei</i>K13 Mutations Mediate<i>In Vivo</i>Artemisinin Resistance That is Reversed by Proteasome Inhibition
<i>Plasmodium berghei</i>K13 Mutations Mediate<i>In Vivo</i>Artemisinin Resistance That is Reversed by Proteasome Inhibition Open
The recent emergence of Plasmodium falciparum (PF) parasite resistance to the first line antimalarial drug artemisinin is of particular concern. Artemisinin resistance is primarily driven by mutations in the PF K13 protein, which enhance s…
View article: Mammalian deubiquitinating enzyme inhibitors display<i>in vitro</i>and<i>in vivo</i>activity against malaria parasites and potentiate artemisinin action
Mammalian deubiquitinating enzyme inhibitors display<i>in vitro</i>and<i>in vivo</i>activity against malaria parasites and potentiate artemisinin action Open
Current malaria control efforts rely significantly on artemisinin combinational therapies which have played massive roles in alleviating the global burden of the disease. Emergence of resistance to artemisinins is therefore, not just alarm…
View article: Experimentally Engineered Mutations in a Ubiquitin Hydrolase, UBP-1, Modulate <i>In Vivo</i> Susceptibility to Artemisinin and Chloroquine in Plasmodium berghei
Experimentally Engineered Mutations in a Ubiquitin Hydrolase, UBP-1, Modulate <i>In Vivo</i> Susceptibility to Artemisinin and Chloroquine in Plasmodium berghei Open
As resistance to artemisinins (current frontline drugs in malaria treatment) emerges in Southeast Asia, there is an urgent need to identify the genetic determinants and understand the molecular mechanisms underpinning such resistance. Such…
View article: Drug action and resistance in malaria parasites: experimental genetics models and biochemical features of fast acting novel antimalarials
Drug action and resistance in malaria parasites: experimental genetics models and biochemical features of fast acting novel antimalarials Open
Resistance to antimalarial drugs inevitably follows their deployment in malaria endemic parts of the world. For instance, current malaria control efforts which significantly rely on artemisinin combination therapies (ACTs) are being threat…
View article: Experimentally engineered mutations in a ubiquitin hydrolase, UBP-1, modulate<i>in vivo</i>resistance to artemisinin and chloroquine in<i>Plasmodium berghei</i>
Experimentally engineered mutations in a ubiquitin hydrolase, UBP-1, modulate<i>in vivo</i>resistance to artemisinin and chloroquine in<i>Plasmodium berghei</i> Open
As resistance to artemisinins (current frontline drugs in malaria treatment) emerges in south East Asia (SEA), there is an urgent need to identify the genetic determinants and understand the molecular mechanisms underpinning such resistanc…
View article: Validation of the protein kinase <i>Pf</i> CLK3 as a multistage cross-species malarial drug target
Validation of the protein kinase <i>Pf</i> CLK3 as a multistage cross-species malarial drug target Open
Targeting parasite's protein kinase Malaria elimination goals are constantly eroded by the challenge of emerging drug and insecticide resistance. Alam et al. have taken established drug targets—CLK protein kinases involved in regulation of…
View article: Validation of the protein kinase <i>PfCLK3</i> as a multi-stage cross species malarial drug target
Validation of the protein kinase <i>PfCLK3</i> as a multi-stage cross species malarial drug target Open
The requirement for next generation anti-malarials to be both curative and transmission blockers necessitate the identification of molecular pathways essential for viability of both asexual and sexual parasite life stages. Here we identify…