Jun Ni
Stanford University
18 Papers
171 Citations
Jun Ni is an academic researcher from Stanford University. The author has contributed to research in topics: Biology & Medicine. The author has an hindex of 8, co-authored 11 publications. Previous affiliations of Jun Ni include University of Michigan & Mayo Clinic.
Chat about Author
Papers
In vivo protein trapping produces a functional expression codex of the vertebrate proteome
Karl J. Clark,Darius Balciunas,Darius Balciunas,Hans Martin Pogoda,Yonghe Ding,Stephanie E. Westcot,Stephanie E. Westcot,Victoria M. Bedell,Tammy M. Greenwood,Mark D. Urban,Kimberly J. Skuster,Andrew M. Petzold,Andrew M. Petzold,Jun Ni,Aubrey L. Nielsen,Ashok Patowary,Vinod Scaria,Sridhar Sivasubbu,Sridhar Sivasubbu,Xiaolei Xu,Matthias Hammerschmidt,Stephen C. Ekker,Stephen C. Ekker +22 more
TL;DR: A conditional in vivo protein-trap mutagenesis system that reveals spatiotemporal protein expression dynamics and can be used to assess gene function in the vertebrate Danio rerio and reports a collection of 350 zebrafish lines that include diverse molecular loci.
Evidence for functional conservation, sufficiency, and proteolytic processing of the CLAVATA3 CLE domain
Jun Ni,Steven E. Clark +1 more
TL;DR: It is proposed that CLV3 and other CLEs are C-terminally processed to generate an active CLE peptide and detected proteolytic activity in extracts from cauliflower that process both CLv3 and CLE1 at their C termini.
180
Mechanisms of molecular mimicry of plant CLE peptide ligands by the parasitic nematode Globodera rostochiensis.
TL;DR: It is demonstrated that GrCLE1 maturation can be entirely carried out by plant factors and that the availability of CLE processing activity may be essential for successful ligand mimicry.
Characterization of a CLE processing activity.
TL;DR: Analysis of an in vitro CLE processing activity is extended and shows that in vitro cleavage occurs at Arg70, exactly matching in vivo maturation, and it is shown that efficient protease recognition can occur with as little as four residues upstream of the CLE domain.
85
Arhgap36-dependent activation of Gli transcription factors
Paul G. Rack,Jun Ni,Alexander Y. Payumo,Vien Nguyen,J. Aaron Crapster,Volker Hovestadt,Marcel Kool,David T.W. Jones,John K. Mich,Ari J. Firestone,Stefan M. Pfister,Yoon Jae Cho,James K. Chen +12 more
TL;DR: A genome-scale cDNA overexpression screen for signaling proteins that promote Gli-dependent transcription reveals a new mechanism of Gli transcription factor activation and implicate ARHGAP36 dysregulation in the onset and/or progression of GLI-dependent cancers.
49