Publications by authors named "M A Solon"
Necroptosis is a lytic form of cell death that is mediated by the kinase RIPK3 and the pseudokinase MLKL when caspase-8 is inhibited downstream of death receptors, toll-like receptor 3 (TLR3), TLR4, and the intracellular Z-form nucleic acid sensor ZBP1. Oligomerization and activation of RIPK3 is driven by interactions with the kinase RIPK1, the TLR adaptor TRIF, or ZBP1. In this study, we use immunohistochemistry (IHC) and in situ hybridization (ISH) assays to generate a tissue atlas characterizing RIPK1, RIPK3, Mlkl, and ZBP1 expression in mouse tissues.
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- T cell-dependent bispecific antibodies (TDBs) not only target tumors but also cause systemic changes that can lead to adverse events in normal organs.
- In animal studies, there was a notable accumulation of lymphocytes and activation of endothelial cells in the liver, while tumor changes were less significant.
- The research suggests that specific genes, including CD9, play a role in enhancing T cell movement into normal tissues, potentially impacting the design of safer and more effective cancer immunotherapies.
We complete the calculation of conservative two-body scattering dynamics at fourth post-Minkowskian order, i.e., O(G^{4}) and all orders in velocity, including radiative contributions corresponding to the tail effect in general relativity.
View Article and Find Full Text PDFInositol requiring enzyme 1 (IRE1) mitigates endoplasmic-reticulum (ER) stress by orchestrating the unfolded-protein response (UPR). IRE1 spans the ER membrane, and signals through a cytosolic kinase-endoribonuclease module. The endoribonuclease generates the transcription factor XBP1s by intron excision between similar RNA stem-loop endomotifs, and depletes select cellular mRNAs through regulated IRE1-dependent decay (RIDD).
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- * A study revealed that the absence of proteins hnRNPC and ADAR together leads to heightened MDA5-dependent IFN responses in monocytes, showcasing a synergistic effect.
- * Findings indicate that hnRNPC deficiency disrupts RNA splicing in Alu-containing introns, leading to reduced editing by ADAR and potentially increasing autoinflammation, suggesting a new direction for immunotherapy in patients with hnRNPC mutations.