Publications by authors named "K Rygiel"

Article Synopsis
  • RNA sequencing and genetic data point to SYK and FCER1G as potential targets for Alzheimer's disease therapy.
  • SYK activates in response to FCER1G interaction, which is linked to worsening AD pathology, leading to the hypothesis that disrupting this interaction could be beneficial.
  • Researchers developed assays to identify small molecules that disrupt the SYK and FCER1G interaction, discovering two chemotypes that inhibit this binding, though they are not selective enough for practical use.
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The past few years have seen exciting discoveries in the area of tyrosine kinase structural biology including the first high resolution models of full-length receptor tyrosine kinases and new mechanistic insights into the structural mechanisms of receptor tyrosine kinase activation. Despite being a mature area of research, the application of new technologies continues to advance our understanding. In this article we highlight a selection of recent studies that illustrate the current areas of research interest, focussing in particular on the exciting progress made possible by cryo-electron-microscopy.

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RNA sequencing and genetic data support spleen tyrosine kinase (SYK) and high affinity immunoglobulin epsilon receptor subunit gamma (FCER1G) as putative targets to be modulated for Alzheimer's disease (AD) therapy. FCER1G is a component of Fc receptor complexes that contain an immunoreceptor tyrosine-based activation motif (ITAM). SYK interacts with the Fc receptor by binding to doubly phosphorylated ITAM (p-ITAM) via its two tandem SH2 domains (SYK-tSH2).

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Obesity has dramatically increased over the past fifty years. In the last decade, it has been noted that augmented body mass, metabolic abnormalities, and the relevant "obese" tumor microenvironment (TME) are connected with signaling molecular networks, which in turn, may contribute to aggressive tumor biology in some patients with breast malignancies. This article presents the associations between obesity, metabolic derangements, inflammatory processes in the adipose tissue or TME, and aggressive behavior of triple-negative breast cancer (TNBC) in African American (AA) women.

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