Publications by authors named "Brett M Condon"

Article Synopsis
  • Over two decades, initiatives have aimed to enhance STEM undergraduate outcomes, with the inclusive Research Education Community (iREC) emerging as a scalable reform model that supports STEM faculty in implementing course-based research to improve student learning.
  • This study utilized pathway modeling to describe the HHMI Science Education Alliance (SEA) iREC, identifying how faculty engagement leads to sustainable adoption and improvement of new teaching strategies through feedback from over 100 participating faculty members.
  • The findings indicate that iREC fosters a collaborative environment where STEM faculty can share expertise and data, thereby enhancing their teaching practices and contributing to the overall evolution of undergraduate science education.
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Course-based research pedagogy involves positioning students as contributors to authentic research projects as part of an engaging educational experience that promotes their learning and persistence in science. To develop a model for assessing and grading students engaged in this type of learning experience, the assessment aims and practices of a community of experienced course-based research instructors were collected and analyzed. This approach defines four aims of course-based research assessment - 1) Assessing Laboratory Work and Scientific Thinking; 2) Evaluating Mastery of Concepts, Quantitative Thinking and Skills; 3) Appraising Forms of Scientific Communication; and 4) Metacognition of Learning - along with a set of practices for each aim.

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Article Synopsis
  • - O-linked β-N-acetylglucosamine (O-GlcNAc) is an important form of glycosylation found in many organisms, crucial for proper cellular function and linked to diseases like cancer and metabolic syndrome.
  • - The study focuses on how O-GlcNAcylation affects the COPII complex, which is vital for transporting proteins from the endoplasmic reticulum in cells.
  • - Researchers discovered new O-GlcNAcylation sites on key COPII proteins and suggest that this glycosylation may be influenced by nutrient levels, linking metabolism with protein trafficking in cells.
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The coat protein complex II (COPII) mediates forward trafficking of protein and lipid cargoes from the endoplasmic reticulum. COPII is an ancient and essential pathway in all eukaryotes and COPII dysfunction underlies a range of human diseases. Despite this broad significance, major aspects of COPII trafficking remain incompletely understood.

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Gigaxonin (also known as KLHL16) is an E3 ligase adaptor protein that promotes the ubiquitination and degradation of intermediate filament (IF) proteins. Mutations in human gigaxonin cause the fatal neurodegenerative disease giant axonal neuropathy (GAN), in which IF proteins accumulate and aggregate in axons throughout the nervous system, impairing neuronal function and viability. Despite this pathophysiological significance, the upstream regulation and downstream effects of normal and aberrant gigaxonin function remain incompletely understood.

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Intermediate filaments (IF) are a major component of the metazoan cytoskeleton and are essential for normal cell morphology, motility, and signal transduction. Dysregulation of IFs causes a wide range of human diseases, including skin disorders, cardiomyopathies, lipodystrophy, and neuropathy. Despite this pathophysiological significance, how cells regulate IF structure, dynamics, and function remains poorly understood.

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The COPII coat complex, which mediates secretory cargo trafficking from the endoplasmic reticulum, is a key control point for subcellular protein targeting. Because misdirected proteins cannot function, protein sorting by COPII is critical for establishing and maintaining normal cell and tissue homeostasis. Indeed, mutations in COPII genes cause a range of human pathologies, including cranio-lenticulo-sutural dysplasia (CLSD), which is characterized by collagen trafficking defects, craniofacial abnormalities, and skeletal dysmorphology.

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