T
Tigwa H. Davis
Researcher at University of Michigan
Publications - 5
Citations - 943
Tigwa H. Davis is an academic researcher from University of Michigan. The author has contributed to research in topics: Neurite & Dicer. The author has an hindex of 5, co-authored 5 publications receiving 897 citations. Previous affiliations of Tigwa H. Davis include University of California, San Francisco.
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Journal ArticleDOI
Conditional Loss of Dicer Disrupts Cellular and Tissue Morphogenesis in the Cortex and Hippocampus
Tigwa H. Davis,Trinna L. Cuellar,Selina M. Koch,Allison J. Barker,Brian D. Harfe,Michael T. McManus,Erik M. Ullian +6 more
TL;DR: In vivo studies of Dicer and miRNAs provide additional support for previous in vitro studies indicating that misregulation of this pathway may result in gross abnormalities in cell number and function that may contribute to a variety of neurological disorders.
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Dicer loss in striatal neurons produces behavioral and neuroanatomical phenotypes in the absence of neurodegeneration
Trinna L. Cuellar,Tigwa H. Davis,Peter T. Nelson,Gabriel B. Loeb,Brian D. Harfe,Erik M. Ullian,Michael T. McManus +6 more
TL;DR: It is shown that dopaminoceptive neurons without Dicer survive over the life of the animal and the lack of profound cell death contrasts with other mouse models in which Dicer has been ablated.
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Voltage-Gated Na+ Channel β1 Subunit-Mediated Neurite Outgrowth Requires Fyn Kinase and Contributes to Postnatal CNS Development In Vivo
William J. Brackenbury,Tigwa H. Davis,Tigwa H. Davis,Chunling Chen,Emily A. Slat,Matthew J. Detrow,Travis L. Dickendesher,Barbara Ranscht,Lori L. Isom +8 more
TL;DR: The results suggest that β1-mediated neurite outgrowth occurs through a lipid raft signaling mechanism that requires the presence of both fyn kinase and contactin, and concludes that voltage-gated Na+ channel β1 subunits signal via multiple pathways on multiple timescales and play important roles in the postnatal development of the CNS.
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Sodium channel β1 subunits promote neurite outgrowth in cerebellar granule neurons
TL;DR: It is demonstrated that homophilic interactions between voltage-gated sodium channel β1 subunits promote neurite extension in cerebellar granule neurons, suggesting a novel role for β1 during neuronal development and the first demonstration of a functional role for sodium channelβ subunit-mediated cell adhesive interactions.
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Identification of the Cysteine Residue Responsible for Disulfide Linkage of Na+ Channel α and β2 Subunits
Chunling Chen,Jeffrey D. Calhoun,Yanqing Zhang,Luis F. Lopez-Santiago,Ningna Zhou,Tigwa H. Davis,James L. Salzer,Lori L. Isom +7 more
TL;DR: It is demonstrated that a single cysteine-to-alanine substitution at extracellular residue Cys-26, located within the immunoglobulin (Ig) domain, abolishes the covalent linkage between α and β2 subunits.