J
Jianming Li
Researcher at University of Michigan
Publications - 95
Citations - 13826
Jianming Li is an academic researcher from University of Michigan. The author has contributed to research in topics: Arabidopsis & Brassinosteroid. The author has an hindex of 45, co-authored 83 publications receiving 12155 citations. Previous affiliations of Jianming Li include Salk Institute for Biological Studies & Chinese Academy of Sciences.
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Journal ArticleDOI
A Putative Leucine-Rich Repeat Receptor Kinase Involved in Brassinosteroid Signal Transduction
Jianming Li,Joanne Chory +1 more
TL;DR: The identification of 18 Arabidopsis dwarf mutants that are unable to respond to exogenously added brassinosteroid, a phenotype that might be expected for brass inosteroid signaling mutants.
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BRI1/BAK1, a Receptor Kinase Pair Mediating Brassinosteroid Signaling
Kyoung Hee Nam,Jianming Li +1 more
TL;DR: It is proposed that BAK1 and BRI1 function together to mediate plant steroid signaling.
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BES1 Accumulates in the Nucleus in Response to Brassinosteroids to Regulate Gene Expression and Promote Stem Elongation
Yanhai Yin,Zhi-Yong Wang,Santiago Mora-García,Jianming Li,Shigeo Yoshida,Tadao Asami,Joanne Chory +6 more
TL;DR: BES1, a semidominant suppressor of bri1, is identified, which exhibits constitutive BR response phenotypes including long and bending petioles, curly leaves, accelerated senescence, and constitutive expression of BR-response genes.
Journal ArticleDOI
A role for brassinosteroids in light-dependent development of Arabidopsis
TL;DR: The Arabidopsis DET2 gene encodes a protein that shares significant sequence identity with mammalian steroid 5α-reductases, and brassinosteroids may constitute a distinct class of phytohormones with an important role in light-regulated development of higher plants.
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The GSK3-like kinase BIN2 phosphorylates and destabilizes BZR1, a positive regulator of the brassinosteroid signaling pathway in Arabidopsis
TL;DR: It is reported that BRs induce dephosphorylation and accumulation of BZR1 protein and that BR signaling causes BzR1 deph phosphorylated and accumulation by inhibiting BIN2 activity.