Publications by authors named "T Kanaji"
Article Synopsis
- * Researchers created a mouse model lacking the nuclear localization signal for TyrRS, leading to decreased lean and fat mass, improved insulin sensitivity, and normal blood sugar levels, pointing to a metabolic role for TyrRS.
- * YARS1 deficiency in mice also resulted in progressive hearing loss, highlighting the importance of TyrRS in fat storage, metabolism, and overall health, emphasizing the connection between protein synthesis and metabolic regulation.
Article Synopsis
- Stress in cells can be signaled in different ways, like using a special protein called eIF2α, which helps stop general protein making but helps the cell survive by activating another factor called ATF4.
- A protein called TyrRS can also help cells respond to stress, but it works later and stops protein making in a different way than eIF2α/ATF4.
- If TyrRS is kept out of the nucleus, it causes too much protein making and can lead to cell death when cells are under a lot of stress for a long time.
Platelets play a role not only in hemostasis and thrombosis, but also in inflammation and innate immunity. We previously reported that an activated form of tyrosyl-tRNA synthetase (YRS) has an extratranslational activity that enhances megakaryopoiesis and platelet production in mice. Here, we report that YRS mimics inflammatory stress inducing a unique megakaryocyte (MK) population with stem cell (Sca1) and myeloid (F4/80) markers through a mechanism dependent on Toll-like receptor (TLR) activation and type I interferon (IFN-I) signaling.
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- * The exact role of these autoantibodies in the development of ASSD is still not fully understood, but they seem to be crucial in the disease's pathogenesis.
- * The study suggests that ASSD may involve the release of aaRSs from cells and highlights the potential role of extracellular tRNAs in triggering immune responses, particularly through Toll-like receptors.