The University of Osaka · Medicine
Professor Kishan Kumar Nyati's research lab focuses on the molecular mechanisms underlying autoimmune and inflammatory diseases, with a central emphasis on posttranscriptional gene regulation, particularly through RNA-binding proteins such as Arid5a. The lab investigates signaling pathways that control mRNA stability and immune response modulation, especially in the context of cytokine regulation (e.g., IL-6) and neuroinflammatory disorders like Guillain-Barré syndrome (GBS). Key research directions include the role of host factors, cytokines, matrix metalloproteinases (MMPs), and microbial triggers (e.g., *Campylobacter jejuni*) in disease pathogenesis and immune dysregulation. The lab integrates molecular immunology, post-transcriptional regulation, and translational research to identify novel therapeutic targets for autoimmune and inflammatory conditions.
Figures are computed from collected data and may differ slightly.
The AT-rich interactive domain-containing protein 5a (Arid5a) plays a critical role in autoimmunity by regulating the half-life of Interleukin-6 (IL-6) mRNA. However, the signaling pathways underlying Arid5a-mediated regulation of IL-6 mRNA stability are largely uncharacterized. Here, we found that during the early phase of lipopolysaccharide (LPS) stimulation, NF-κB and an NF-κB-triggered IL-6-positive feedback loop activate Arid5a gene expression, increasing IL-6 expression via stabilization o
Our current knowledge on Campylobacter jejuni infections in humans has progressively increased over the past few decades. Infection with C. jejuni is the most common cause of bacterial gastroenteritis, sometimes surpassing other infections due to Salmonella, Shigella, and Escherichia coli. Most infections are acquired due to consumption of raw or undercooked poultry, unpasteurized milk, and contaminated water. After developing the diagnostic methods to detect C. jejuni, the possibility to identi
Upregulation of T(H)1 cytokines in the early disease course may be associated with immune-mediated disease progression due to neuronal inflammation, but upregulation of T(H)2 immune response during the later phase aids recovery from the disease.
Abnormal gene expression patterns underlie many diseases that represent major public health concerns and robust therapeutic challenges. Posttranscriptional gene regulation by RNA-binding proteins (RBPs) is well-recognized, and the biological functions of RBPs have been implicated in many diseases, such as autoimmune diseases, inflammatory diseases, and cancer. However, a complete understanding of the regulation mediated by several RBPs is lacking. During the past few years, a novel role of AT-ri
Guillain-Barré syndrome (GBS) is an autoimmune disease of the peripheral nervous system, mostly triggered by an aberrant immune response to an infectious pathogen. Although several infections have been implicated in the pathogenesis of GBS, not all such infected individuals develop this disease. Moreover, infection with a single agent might also lead to different subtypes of GBS emphasizing the role of host factors in the development of GBS. The host factors regulate a broad range of inflammator
The role of matrix metalloproteinases (MMPs) and cytokines in the pathogenesis of Guillain-Barré syndrome (GBS) largely remains unknown. We studied the role of MMP-2, MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in disease progression and recovery of patients with GBS. Sixty-five patients with GBS and 68 healthy controls were enrolled in the study. Serum levels of MMP-2, MMP-9, TNF-α, and IL-1β were analyzed by ELISA, and activities of MMPs were measured by zymography. Expr
AT-rich interactive domain 5a (Arid5a) is a nucleic acid binding protein. In this review, we highlight recent advances in the association of Arid5a with inflammation and human diseases. Arid5a is known as a protein that performs dual functions. In <i>in vitro</i> and <i>in vivo</i> studies, it was found that an inflammation-dependent increase in Arid5a expression mediates both transcriptional and post-transcriptional regulatory effects that are implicated in immune regulation and cellular homeos
AT-rich interactive domain 5a (Arid5a) is a member of the arid family of proteins, which contain a helix-turn-helix domain and an ability to bind to nucleic acids. Current evidence suggests that Arid5a performs dual functions as a transcription factor and an RNA-binding protein in immune, nonimmune, and/ or tumor cells depending on its cellular localization. The contribution of Arid5a to the development of inflammation, autoimmunity, and obesity through its transcriptional and posttranscriptiona
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