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Vijay K. Gonugunta

Researcher at University of Texas Health Science Center at San Antonio

Publications -  14
Citations -  1904

Vijay K. Gonugunta is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Abscisic acid & Guard cell. The author has an hindex of 14, co-authored 14 publications receiving 1523 citations. Previous affiliations of Vijay K. Gonugunta include University of Texas Southwestern Medical Center & University of Hyderabad.

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Journal ArticleDOI

ABA perception and signalling.

TL;DR: This work has shown a unique hormone perception mechanism where binding of ABA to the ABA receptors RCARs/PYR1/PYLs leads to inactivation of type 2C protein phosphatases such as ABI1 and ABI2 which targets ABA-dependent gene expression and ion channels.
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Trafficking-Mediated STING Degradation Requires Sorting to Acidified Endolysosomes and Can Be Targeted to Enhance Anti-tumor Response

TL;DR: It is shown that trafficking-mediated STING degradation requires ER exit and function of vacuolar ATPase complex and the helix amino acid 281 (aa281)-297 as a motif required for trafficking- mediated STing degradation.
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Nitric oxide production occurs downstream of reactive oxygen species in guard cells during stomatal closure induced by chitosan in abaxial epidermis of Pisum sativum.

TL;DR: itosan strike a marked similarity with those of ABA or MJ on guard cells and indicate the convergence of their signal transduction pathways leading to stomatal closure, and it is proposed that the production of NO is an important signaling component and participates downstream of ROS production.
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STING-associated vasculopathy develops independently of IRF3 in mice

TL;DR: The SAVI-associated STING N153S mutation triggers IRF3-independent immune cell dysregulation and lung disease in mice and causes myeloid cell expansion, T cell cytopenia, and dysregulation of immune cell signaling.
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Nitric oxide production occurs after cytosolic alkalinization during stomatal closure induced by abscisic acid

TL;DR: It is suggested that during ABA-induced stomatal closure, a rise in cytosolic pH is necessary for NO production, besides its known function as a downstream component, which may act upstream of cytosol alkalinization and NO production.