Publications by authors named "N A Grieshaber"

Article Synopsis
  • Bacteria from the genus Chlamydia are harmful to both humans and animals, causing diseases like pneumonia and infections in the genital and ocular regions.
  • These bacteria are obligate intracellular parasites that rely on a complex life cycle involving different stages: the elementary body (EB) for infection, the reticulate body (RB) for replication, and the intermediate body (IB) for transition between these forms.
  • A study showed that high levels of the regulatory protein Euo can halt the bacteria's developmental cycle at the IB stage, affecting their ability to mature into the infectious EB form, but this pause can be reversed by lowering Euo levels.
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Diseases caused by spp. are often associated with persistent infections. Chlamydial persistence is commonly associated with a unique non-infectious intracellular developmental form, termed an aberrant form.

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Chlamydia trachomatis is an obligate intracellular bacterium that progresses through an essential multicell form developmental cycle. Infection of the host is initiated by the elementary body (EB). Once in the host, the EB cell differentiates into the noninfectious, but replication-competent, reticulate body, or RB.

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Chlamydia trachomatis is a bacterial obligate intracellular parasite and a significant cause of human disease, including sexually transmitted infections and trachoma. The bacterial RNA polymerase-binding protein DksA is a transcription factor integral to the multicomponent bacterial stress response pathway known as the stringent response. The genome of C.

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The human pathogen Chlamydia trachomatis proceeds through a multi phenotypic developmental cycle with each cell form specialized for different roles in pathogenesis. Understanding the mechanisms regulating this complex cycle has historically been hampered by limited genetic tools. In an effort to address this issue, we developed a translational control system to regulate gene expression in Chlamydia using a synthetic riboswitch.

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