Results 181 to 190 of about 253,061 (341)
Induction of IL-5 expression by IL-2 is resistant to the immunosuppressive agents cyclosporin A and rapamycin [PDF]
Janet E. Valentine
openalex +1 more source
By catalyzing FAM134B ubiquitination and activating ER‐phagy, AMFR alleviates progressive fibrosis and cardiac dysfunction by inhibiting the mTORC1 pathway. Consequently, these findings underscore the essential role of AMFR‐driven ER‐phagy in mitigating the progression of fibrotic responses, offering a potential therapeutic target for preventing heart ...
Zhixiang Wang+10 more
wiley +1 more source
Abstract Epilepsy syndromes during the early years of life may be attributed to an acquired insult, such as hypoxic–ischemic injury, infection, status epilepticus, or brain trauma. These conditions are frequently modeled in experimental rodents to delineate mechanisms of epileptogenesis and investigate novel therapeutic strategies.
Anna‐Maria Katsarou+7 more
wiley +1 more source
The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis
This review summarizes recent advances in understanding the immune microenvironment's role in fibrosis, focusing on phenotypic/functional alterations of immune cells and their dynamic interactions with other cellular constituents within tissues. The authors further explore therapeutic opportunities and challenges in targeting immune microenvironment ...
Xiangqi Chen+6 more
wiley +1 more source
The transcriptional profile of Saccharomyces cerevisiae exposed to rapamycin mimics the profile induced by amino acid starvation [PDF]
James S. Hardwick+2 more
openalex +1 more source
DNA‐Based Genetic and Non‐Genetic Tools for Receptor Engineering. This review highlights recent advances in DNA‐based strategies for receptor engineering, including genetic approaches like domain fusion and site‐directed mutagenesis, as well as non‐genetic methods using functional nucleic acids, DNA nanostructures, and dynamic DNA reactions.
Hexin Nan+4 more
wiley +1 more source
Ovarian cancer patients with high levels of mortalin protein in their tumors have worse survival. The investigational drug SHetA2 interferes with mortalin's support of mitochondria. The resulting mitochondrial damage causes a process called mitophagy that contributes to how SHetA2 kills cancer cells. Noncancerous cells repair their mitochondria through
Vishal Chandra+9 more
wiley +1 more source