Publications by authors named "James M McCoy"

Article Synopsis
  • * Research shows that ATP4 is located in the plasma membrane and is crucial for regulating cytosolic Na concentration; its inhibition leads to a rise in Na and increased alkalinity in the cells.
  • * Knockdown of ATP4 impairs parasite growth and virulence in mice, highlighting its essential role in maintaining Na balance for the survival and function of these parasites.
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The proper ablation of any neoplasm of the head and neck requires the inclusion of linear and anatomic barrier margins surrounding the neoplasm. Extirpative surgery of the major and minor salivary glands is certainly no exception to this surgical principle. To this end, the selection and execution of the most appropriate ablative surgical procedure for a major or minor benign salivary gland neoplasm is an essential exercise in oral and maxillofacial surgery.

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Type III secretion systems (T3SSs) are protein transport nanomachines that are found in Gram-negative bacterial pathogens and symbionts. Resembling molecular syringes, T3SSs form channels that cross the bacterial envelope and the host cell membrane, which enable bacteria to inject numerous effector proteins into the host cell cytoplasm and establish trans-kingdom interactions with diverse hosts. Recent advances in cryo-electron microscopy and integrative imaging have provided unprecedented views of the architecture and structure of T3SSs.

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, like all apicomplexan parasites, uses Ca signaling pathways to activate gliding motility to power tissue dissemination and host cell invasion and egress. A group of "plant-like" Ca-dependent protein kinases (CDPKs) transduces cytosolic Ca flux into enzymatic activity, but how they function is poorly understood. To investigate how Ca signaling activates egress through CDPKs, we performed a forward genetic screen to isolate gain-of-function mutants from an egress-deficient knockout strain.

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Transmissible stages of Toxoplasma gondii store energy in the form of the carbohydrate amylopectin. Here, we show that the Ca(2+)-dependent protein kinase CDPK2 is a critical regulator of amylopectin metabolism. Increased synthesis and loss of degradation of amylopectin in CDPK2 deficient parasites results in the hyperaccumulation of this sugar polymer.

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The phylum Apicomplexa comprises a group of obligate intracellular parasites of broad medical and agricultural significance, including Toxoplasma gondii and the malaria-causing Plasmodium spp. Key to their parasitic lifestyle is the need to egress from an infected cell, actively move through tissue, and reinvade another cell, thus perpetuating infection. Ca(2+)-mediated signaling events modulate key steps required for host cell egress, invasion and motility, including secretion of microneme organelles and activation of the force-generating actomyosin-based motor.

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Translational repression is important for development of the malaria parasite when establishing infection in the mosquito. In this issue of Cell Host and Microbe, Sebastian et al. (2012) show that a calcium-dependent protein kinase is important for alleviating translational repression during developmental progression.

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