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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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Candidate downstream regulated genes of HOX group 13 transcription factors with and without monomeric DNA binding capability.

TL;DR: The results suggest that HOX protein-protein interactions without direct HOX DNA-binding may play a larger role in HOX transcriptional regulation than generally assumed, and DNA- binding appears critical for repression.
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Dax1 Up-Regulates Oct4 Expression in Mouse Embryonic Stem Cells via LRH-1 and SRA

TL;DR: Dax1 plays an important role in the maintenance of pluripotency in mES cells through interaction with LRH-1 and transcriptional activation of Oct4 and other genes.
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Profiling of pathway-specific changes in gene expression following growth of human cancer cell lines transplanted into mice

TL;DR: Studies of this type allow us to examine the specific contribution of cancer cells to gene expression patterns within an in vivo tumor mixed with non-cancerous tissue.
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Inhibition of histone methylation arrests ongoing graft-versus-host disease in mice by selectively inducing apoptosis of alloreactive effector T cells

TL;DR: In vivo administration of the histone methylation inhibitor 3-deazaneplanocin A (DZNep) arrests ongoing GVHD in mice after allogeneic BM transplantation and preserves the antileukemia activity of donor T cells and did not impair the recovery of hematopoiesis and lymphocytes, leading to significantly improved survival of recipients after allogenicic BM transplation.
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Intra-tumor genetic heterogeneity in rectal cancer

TL;DR: The occurrence of significant intra-tumor heterogeneity in rectal cancers involving variations in localized somatic mutations and copy number abnormalities may allow selected tumors to have a genetic reservoir to draw from in their evolutionary response to therapy and other challenges.