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Rita Bortell

Researcher at University of Massachusetts Medical School

Publications -  61
Citations -  3533

Rita Bortell is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Insulin & Islet. The author has an hindex of 29, co-authored 61 publications receiving 3197 citations. Previous affiliations of Rita Bortell include National Institutes of Health & University of Massachusetts Amherst.

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Regulation of insulin biosynthesis in pancreatic beta cells by an endoplasmic reticulum-resident protein kinase IRE1

TL;DR: IRE1 signaling activated by transient exposure to high glucose uses a unique subset of downstream components and has a beneficial effect on pancreatic beta cells, and is a potential target for therapeutic regulation of insulin biosynthesis.
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Human peripheral blood leucocyte non-obese diabetic-severe combined immunodeficiency interleukin-2 receptor gamma chain gene mouse model of xenogeneic graft-versus-host-like disease and the role of host major histocompatibility complex.

TL;DR: A robust model of xenogeneic graft‐versus‐host‐like disease (GVHD) based on intravenous injection of human PBMC into 2 Gy conditioned NOD‐scid IL2rγnull mice is reported, and interrupting the tumour necrosis factor‐α signalling cascade with etanercept delays the onset and progression of disease.
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Rat models of type 1 diabetes: genetics, environment, and autoimmunity.

TL;DR: Data generated in the rat have correctly predicted the outcome of several human diabetes prevention trials, notably the failure of nicotinamide and low dose parenteral and oral insulin therapies.
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Coordinate occupancy of AP-1 sites in the vitamin D-responsive and CCAAT box elements by Fos-Jun in the osteocalcin gene: model for phenotype suppression of transcription

TL;DR: Results support a model in which coordinate occupancy of the AP-1 sites in the VDRE and OC box in proliferating osteoblasts may suppress both basal level and vitamin D-enhanced osteocalcin gene transcription as well as transcription of other genes associated with osteoblast differentiation--a phenomenon the authors describe as phenotype suppression.