Publications by authors named "Megan Mazzei"

Article Synopsis
  • - The RAS family GTPases are a key group of oncogenes frequently mutated in human cancers, with mutations found in about 20% of tumors, particularly NRAS mutations present in about 25% of melanomas.
  • - Current therapies have targeted KRAS mutations effectively, but there is a significant lack of treatments specifically aimed at NRAS, making it a critical area for developing new cancer therapies.
  • - This study introduces a new monobody that can bind to both forms of NRAS and inhibit its signaling, offering a promising direction for creating selective inhibitors and potential therapeutics for NRAS and BRAF-mutant melanomas.
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Mutations in one of the three RAS genes (HRAS, KRAS, and NRAS) are present in nearly 20% of all human cancers. These mutations shift RAS to the GTP-loaded active state due to impairment in the intrinsic GTPase activity and disruption of GAP-mediated GTP hydrolysis, resulting in constitutive activation of effectors such as RAF. Because activation of RAF involves dimerization, RAS dimerization has been proposed as an important step in RAS-mediated activation of effectors.

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The mycobacteriophages JeTaime (E cluster) and Luna22 (Q cluster) were isolated from soil in Providence, Rhode Island, and Charleston, South Carolina, respectively, using a Mycobacterium smegmatis mc 155 host. The genome of JeTaime is 75,099 bp (142 predicted genes), and that of Luna22 is 53,730 bp (87 predicted genes). Both phages exhibit morphology.

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