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Xiaodi Hu
Researcher at University of Massachusetts Medical School
Publications - 20
Citations - 909
Xiaodi Hu is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 6, co-authored 7 publications receiving 801 citations.
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Journal ArticleDOI
Toll and IMD Pathways Synergistically Activate an Innate Immune Response in Drosophila melanogaster
TL;DR: It is shown that the Toll and IMD pathways can interact synergistically, demonstrating that cross-regulation occurs and illustrating how specific ligand binding by separate upstream pattern recognition receptors can be translated into a broad-spectrum host response, a hallmark of innate immunity.
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A Conserved p38 Mitogen-Activated Protein Kinase Pathway Regulates Drosophila Immunity Gene Expression
Zhiqiang Stanley Han,Hervé Enslen,Xiaodi Hu,Xiangjun Meng,I-Huan Wu,Tamera Barrett,Roger J. Davis,Y. Tony Ip +7 more
TL;DR: The results revealed that one of the functions of D-p38 is to attenuate antimicrobial peptide gene expression following exposure to lipopolysaccharide, establishing that Drosophilaindeed possesses a conserved p38 MAP kinase signaling pathway.
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Multimerization and interaction of Toll and Spätzle in Drosophila.
TL;DR: The results suggest that multimerization may be a regulated, essential step for Toll-receptor activation, and that constitutively active mutants of Toll form multimers that contain intermolecular disulfide linkages.
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The Drosophila Toll-9 activates a constitutive antimicrobial defense.
TL;DR: The results suggest that Toll‐9 is a constitutively active protein, and implies its novel function in protecting the host by maintaining a substantial level of antimicrobial gene products to ward off the continuous challenge of microorganisms.
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The mesoderm determinant snail collaborates with related zinc-finger proteins to control Drosophila neurogenesis.
TL;DR: Transgenic expression of each of the three Snail family proteins can rescue efficiently the fushi tarazu defects, and partially the pdm‐2 and even‐skipped CNS patterns.