PfKIN, an SNF1 type protein kinase of Plasmodium falciparum predominantly expressed in gametocytes

Bracchi, Valérie; Langsley, Gordon; Thélu, Jacques; Eling, W.M.C.; Ambroise-Thomas, P

doi:10.1016/0166-6851(96)02564-9

Cited by 19 publications

(11 citation statements)

References 18 publications

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“…Examples of such "orphan" kinases are (i) the cluster formed by PfKIN [PF140516], an enzyme previously described as related to the SNF1 family [42], with two uncharacterised PfPKs [PF14_0476 and PF13_0085]. This cluster is located at the base of the CamK and AGC branches, and does not strongly associate with any established ePK group (when mammalian NIM1/SNF1-like kinases were included in the phylogenetic tree no malarial kinases clustered with them (not shown)).…”

Section: Resultsmentioning

confidence: 99%

“…Compilation of data from this study indicated that a small number of PfePKs are specific to gametocytes, including two of the NIMA-related kinases (one of which is potentially targeted to the apicoplast), one of the MAPKs (Pfmap-2), and PfKIN, an enzyme previously described as related to the SNF1 family (see above). Gametocyte-specific expression had been described in the literature for the latter two enzymes [42,45]. Overall, and despite some discrepancies, there is good agreement between the two studies with respect to PfePK genes, as illustrated by the observation that PfePKs whose expression is detected in late schizonts and segmenters by Bozdech et al are also detected in free merozoites by Le Roch et al At least some of these enzymes are likely to play a role in invasion of the erythrocyte by the merozoite.…”

Section: Resultsmentioning

confidence: 99%

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Protein kinases of the human malaria parasite Plasmodium falciparum: the kinome of a divergent eukaryote

et al. 2004

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Background: Malaria, caused by the parasitic protist Plasmodium falciparum, represents a major public health problem in the developing world. The P. falciparum genome has been sequenced, which provides new opportunities for the identification of novel drug targets. Eukaryotic protein kinases (ePKs) form a large family of enzymes with crucial roles in most cellular processes; hence malarial ePKS represent potential drug targets. We report an exhaustive analysis of the P. falciparum genomic database (PlasmoDB) aimed at identifying and classifying all ePKs in this organism.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Protein kinases of the human malaria parasite Plasmodium falciparum: the kinome of a divergent eukaryote

et al. 2004

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“…Yeast SNF1 plays a role in transcriptional activation and repression to respond to several forms of stress such as nutrient limitation, salt stress and heat shock (reviewed in [47,48]). PfKIN is predominantly expressed in gametocytes [49], and accordingly reverse genetics in P. berghei indicates that the gene product is not required for the erythrocytic asexual cycle.…”

Section: The Camk Groupmentioning

confidence: 99%

The kinomes of apicomplexan parasites

Miranda‐Saavedra

Gabaldón

Barton

et al. 2012

Microbes and Infection

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Protein phosphorylation plays a fundamental role in the biology and invasion strategies of apicomplexan parasites. Many apicomplexan protein kinases are substantially different from their mammalian orthologues, and thus constitute a landscape of potential drug targets. Here, we integrate genomic, biochemical, genetic and evolutionary information to provide an integrated and up-to-date analysis of twelve apicomplexan kinomes. All kinome sequences are available through the Kinomer database.2

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“…KIN is a putative serine/threonine kinase, with limited homology to the conserved family of sucrose non-fermenting 1 (SNF1) and AMP-activated kinases (AMPK)4,14,17 that regulate cellular energy homeostasis in yeast and mammalian cells, respectively18,19. AMPK/SNF1 is a heterotrimeric complex comprising a α-catalytic subunit and two regulatory subunits β and γ.…”

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confidence: 99%

Nutrient sensing modulates malaria parasite virulence

Mâncio-Silva

Slavic

Ruivo

et al. 2017

Nature

162

161

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The lifestyle of intracellular pathogens, such as malaria parasites, is intimately connected to that of their host(s), primarily for nutrient supply. Nutrients act not only as primary sources of energy but also as regulators of gene expression, metabolism and growth, through various signaling networks that confer to cells the ability to sense and adapt to varying environmental conditions1,2. Canonical nutrient-sensing pathways are presumably absent in the causing agent of malaria Plasmodium3–5, thus raising the question of whether these parasites possess the capacity to sense and cope with host nutrient fluctuations. Here, we show that Plasmodium blood-stage parasites actively respond to host dietary calorie alterations through a rearrangement of their transcriptome accompanied by a significant adjustment of their multiplication rate. A kinome analysis combined with chemical and genetic approaches identified KIN as a critical regulator that mediates sensing of nutrients and controls a transcriptional response to the host nutritional status. KIN shares homology to SNF1/AMPKα and yeast complementation studies suggest functional conservation of an ancient cellular energy sensing pathway. Overall, these findings reveal a key parasite nutrient-sensing mechanism that is critical to modulate parasite replication and virulence.

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PfKIN, an SNF1 type protein kinase of Plasmodium falciparum predominantly expressed in gametocytes

Cited by 19 publications

References 18 publications

Protein kinases of the human malaria parasite Plasmodium falciparum: the kinome of a divergent eukaryote

Protein kinases of the human malaria parasite Plasmodium falciparum: the kinome of a divergent eukaryote

The kinomes of apicomplexan parasites

Nutrient sensing modulates malaria parasite virulence

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