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Rork Kuick

Researcher at University of Michigan

Publications -  166
Citations -  17557

Rork Kuick is an academic researcher from University of Michigan. The author has contributed to research in topics: Gene & Gene expression profiling. The author has an hindex of 60, co-authored 166 publications receiving 16459 citations. Previous affiliations of Rork Kuick include University of Florida.

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Familial molar tissues due to mutations in the inflammatory gene, NALP7, have normal postzygotic DNA methylation.

TL;DR: This study assesses the extent of abnormal DNA methylation in two HMs caused by mutations in the recently identified 19q13.4 gene, NALP7, and demonstrates normal postzygoticDNA methylation patterns at major repetitive and long interspersed nuclear elements, genes on the inactive X-chromosome, three-cancer related genes, and CpG rich regions surrounding the PEG3 differentially methylated region (DMR).
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Low-volume, high-throughput sandwich immunoassays for profiling plasma proteins in mice: identification of early-stage systemic inflammation in a mouse model of intestinal cancer.

TL;DR: This method was used to profile the levels of 14 different cytokines, acute‐phase reactants, and other cancer markers in plasma from mouse models of intestinal tumors and their wild‐type littermates, using as little as 1.5μl of diluted plasma per assay.
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Diminished phosphorylation of a heat shock protein (HSP 27) in infant acute lymphoblastic leukemia.

TL;DR: It is concluded that leukemic cells in infant ALL exhibit a unique pattern of phosphorylation of hsp27 expressed at a pre-B cell stage of differentiation.
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Analysis of human peripheral blood T cells and single-cell-derived T cell clones uncovers extensive clonal CpG island methylation heterogeneity throughout the genome

TL;DR: Qualitative analysis of two-dimensional DNA patterns suggests extensive diversity in vivo in the methylation and expression profiles of individual T cells at multiple unrelated loci across the genome.
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Estimation of mutation rates based on the analysis of polypeptide constituents of cultured human lymphoblastoid cells.

TL;DR: An excess of structural gene mutations at ten known polymorphic loci and repeat mutations at these and other loci suggest nonrandomness of mutation in human somatic cells, and nullimorphs occurring at three heterozygous loci in TK-6 cells may be caused by genetic processes other than structural gene mutation.