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John J. Grant

Researcher at University of California, Berkeley

Publications -  7
Citations -  1980

John J. Grant is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Arabidopsis & Mutant. The author has an hindex of 7, co-authored 7 publications receiving 1762 citations.

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Two calcineurin B-like calcium sensors, interacting with protein kinase CIPK23, regulate leaf transpiration and root potassium uptake in Arabidopsis.

TL;DR: Results imply that plasma membrane-localized CBL1- and CBL9-CIPK23 complexes simultaneously regulate K+ transport processes in roots and in stomatal guard cells.
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CBL1, a calcium sensor that differentially regulates salt, drought, and cold responses in Arabidopsis.

TL;DR: It is suggested that CBL1 functions as a positive regulator of salt and drought responses and a negative regulator of cold response in plants.
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CIPK3, a Calcium Sensor–Associated Protein Kinase That Regulates Abscisic Acid and Cold Signal Transduction in Arabidopsis

TL;DR: It is shown that CIPK3, a Ser/Thr protein kinase that associates with a calcineurin B–like calcium sensor, regulates ABA response during seed germination and ABA- and stress-induced gene expression in Arabidopsis.
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The calcium sensor calcineurin B-like 9 modulates abscisic acid sensitivity and biosynthesis in Arabidopsis.

TL;DR: Analysis of the cbl9 mutant plants showed enhanced expression of genes involved in ABA signaling, such as ABA-INSENSITIVE 4 and 5, and increased stress sensitivity in the mutant may be a result of both ABA hypersensitivity and increased accumulation of ABA under the stress conditions.
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ABR1, an APETALA2-Domain Transcription Factor That Functions as a Repressor of ABA Response in Arabidopsis

TL;DR: An APETALA2 (AP2) domain transcription factor is identified that serves as a repressor of ABA response during seed germination and ABA- and stress-induced gene expression in Arabidopsis (Arabidopsis thaliana) and increased stress sensitivity may result from hypersensitivity to ABA as ABA biosynthesis inhibitor rescued the stress hypersensitivity phenotype.