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Rachel D. Melamed

Researcher at University of Chicago

Publications -  22
Citations -  3411

Rachel D. Melamed is an academic researcher from University of Chicago. The author has contributed to research in topics: Health care & Medicine. The author has an hindex of 12, co-authored 17 publications receiving 3051 citations. Previous affiliations of Rachel D. Melamed include Columbia University Medical Center & Brigham and Women's Hospital.

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Single-Cell Mass Cytometry of Differential Immune and Drug Responses Across a Human Hematopoietic Continuum

TL;DR: Single-cell “mass cytometry” analyses provide system-wide views of immune signaling in healthy human hematopoiesis, against which drug action and disease can be compared for mechanistic studies and pharmacologic intervention.
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Foxp3 Transcription-Factor-Dependent and -Independent Regulation of the Regulatory T Cell Transcriptional Signature

TL;DR: A cross-sectional analysis of the Treg cell signature in Treg-like cells generated under a number of conditions is performed to delineate the elements that can be ascribed to T cell activation, interleukin-2, transforming growth factor-beta (TGF-beta) signaling, or Foxp3 itself.
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A Nondegenerate Code of Deleterious Variants in Mendelian Loci Contributes to Complex Disease Risk

TL;DR: Using genome-wide association results, it is demonstrated that common variants associated with complex diseases are enriched in the genes indicated by this "Mendelian code," illustrating a complementary approach for mapping complex disease loci and providing unique predictions concerning the etiologies of specific diseases.
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Sustained antigen presentation can promote an immunogenic T cell response, like dendritic cell activation

TL;DR: It is shown that either prolonged antigen presentation or DC activation could elicit full expansion, effector cytokine production, and memory-cell differentiation in dendritic cells, suggesting that antigen persistence may be an important discriminator of immunogenic and tolerogenic antigen exposure.
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FBXW7 Mutations in Melanoma and a New Therapeutic Paradigm

TL;DR: Evidence is provided on FBXW7 as a critical tumor suppressor mutated and inactivated in melanoma that results in sustained NOTCH1 activation and renders NOTCH signaling inhibition as a promising therapeutic strategy in this setting.