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Nancy A. Jenkins

Researcher at Houston Methodist Hospital

Publications -  743
Citations -  105243

Nancy A. Jenkins is an academic researcher from Houston Methodist Hospital. The author has contributed to research in topics: Gene & Gene mapping. The author has an hindex of 155, co-authored 741 publications receiving 101587 citations. Previous affiliations of Nancy A. Jenkins include Institute of Molecular and Cell Biology & University of Texas MD Anderson Cancer Center.

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Targeted inactivation of Kinesin-1 in pancreatic β-cells in vivo leads to insulin secretory deficiency

TL;DR: In addition to being essential for maintaining glucose homeostasis and regulatingβ-cell function, Kif5b may be involved in β-cell development by regulating β- cell proliferation and insulin vesicle synthesis.
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Cloning and structure of the human corticotrophin releasing factor-binding protein gene (CRHBP)

TL;DR: The human CRF-binding protein gene has been cloned and mapped to the distal region of chromosome 13 and loci 5q in the mouse and human genomes, respectively.
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Comparative genetics and evolution of annexin A13 as the founder gene of vertebrate annexins

TL;DR: The unique, conserved aspects of annexin A13 primary structure, gene organization, and genetic maps identify it as the probable common ancestor of all vertebrate annexins, beginning with the sequential duplication to annexins A7 and A11 approximately 700 MYA, before the emergence of chordates.
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Structural characterization and chromosomal location of the mouse macrophage migration inhibitory factor gene and pseudogenes

TL;DR: The structure and chromosomal location of the mouse Mif gene and the partial characterization of five Mif pseudogenes suggest that Mif Pseudogenes originated by retrotransposition.
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The Role of MITF Phosphorylation Sites During Coat Color and Eye Development in Mice Analyzed by Bacterial Artificial Chromosome Transgene Rescue

TL;DR: It is shown that mice that carry a BAC transgene where single-amino-acid substitutions have been made in the Mitf gene rescue the phenotype of the loss-of-function mutations in Mitf, which may indicate that signaling from KIT to MITF affects other phospho-acceptor sites in MITF or that alternative sites can be phosphorylated when Ser73 and Ser409 have been mutated.