T
Thomas Su
Researcher at University of Washington
Publications - 8
Citations - 1340
Thomas Su is an academic researcher from University of Washington. The author has contributed to research in topics: Signal transduction & Cre recombinase. The author has an hindex of 8, co-authored 8 publications receiving 1130 citations. Previous affiliations of Thomas Su include University of California, Los Angeles.
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Journal ArticleDOI
Cell-type-specific isolation of ribosome-associated mRNA from complex tissues
TL;DR: A strategy to rapidly and efficiently isolate ribosome-associated mRNA transcripts from any cell type in vivo is described and the application of this technique is demonstrated in brain using neuron-specific Cre recombinase-expressing mice and in testis using a Sertoli cell Cre recomb inase- expressing mouse.
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Mutation of the Cα Subunit of PKA Leads to Growth Retardation and Sperm Dysfunction
Bjørn S. Skålhegg,Yongzhao Huang,Thomas Su,Rejean L. Idzerda,G. Stanley McKnight,Kimberly A. Burton +5 more
TL;DR: Analysis of sperm in Calpha knockout males revealed that spermatogenesis progressed normally but that mature sperm had defective forward motility, and growth retardation was not due to decreased GH production but did correlate with a reduction in IGF-I mRNA in the liver and diminished production of the major urinary proteins in kidney.
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Protein kinase C family functions in B-cell activation
TL;DR: Evidence indicates that PKCbeta might regulate inhibitor of kappaB kinase (IKK) and NF-kappaB activation through interaction with the CARMA1/Bcl10/MALT signaling complex in BCR microdomains.
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Increased Basal cAMP-dependent Protein Kinase Activity Inhibits the Formation of Mesoderm-derived Structures in the Developing Mouse Embryo
Paul S. Amieux,Douglas G. Howe,Heidi Knickerbocker,David C. Lee,Thomas Su,George S. Laszlo,Rejean L. Idzerda,G. Stanley McKnight +7 more
TL;DR: It is demonstrated that unregulated PKA activity negatively affects growth factor-mediated mesoderm formation during early mouse development and can be completely rescued by crossing RIα mutants to mice carrying a targeted disruption in the Cα catalytic subunit.
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Mutations in AKAP5 disrupt dendritic signaling complexes and lead to electrophysiological and behavioral phenotypes in mice.
Michael Weisenhaus,Margaret L. Allen,Linghai Yang,Yuan Lu,C. Blake Nichols,Thomas Su,Johannes W. Hell,G. Stanley McKnight +7 more
TL;DR: The results indicate that the targeting of calcineurin or other binding partners of AKAP5 in the absence of the balancing kinase, PKA, leads to a disruption of synaptic plasticity and results in learning and memory defects.