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Raymond J. MacDonald

Researcher at University of Texas Southwestern Medical Center

Publications -  124
Citations -  31069

Raymond J. MacDonald is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Gene expression & Pancreas. The author has an hindex of 56, co-authored 121 publications receiving 30650 citations. Previous affiliations of Raymond J. MacDonald include University of Pennsylvania & Howard Hughes Medical Institute.

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Journal ArticleDOI

Oestrogen administration and the expression of the kallikrein gene family in the rat submandibular gland

TL;DR: A tissue-specificity in the oestrogen regulation of true kallikrein gene expression in the two tissues is suggested, consistent with the previously reported androgen dependence of SMG expression of these genes with the exception of PS.
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Pancreas-specific genes: structure and expression.

TL;DR: These experiments demonstrate that amylase mRNA is present in all acinar cells but not in other pancreatic cell types, and proposes an extended gene structure 10 kilobase pairs in length containing the 1547 base pairs of the cloned mRNA coding sequence interrupted by seven intervening sequences ranging from 400–2000 base pairs long.
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Computer aided prediction and evaluation of the tertiary structure for rat elastase II

TL;DR: Predictive methods have been extended to generate a proposed tertiary structure of rat elastase II on the basis of primary amino acid sequence and structural homologies within the family of mammalian serine proteinases that suggests probable substrate cleavage preferences.
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Ptf1a control of Dll1 reveals an alternative to the lateral inhibition mechanism

TL;DR: There was an error published in Development 139, where p. 36, Fig. 1 was incorrectly cited several times in place of Fig. 2.
Posted ContentDOI

Prevention and reversion of pancreatic tumorigenesis through a differentiation-based mechanism

TL;DR: It is demonstrated that maintained activity of Ptf1a is sufficient to eliminate Kras-driven tumorigenesis, even in the presence of tumor-promoting inflammation, and that reactivation of an endogenous differentiation program can prevent and reverse oncogenesis in cells harboring tumor driving mutations.