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Lung cancer associated transcript 1 (LUCAT1) is a long noncoding RNA and has been identified as a negative feedback regulator of interferon I and inflammatory cytokine expression in myeloid cells; the anti-inflammatory protein nuclear receptor 4A2 (NR4A2) was identified as a LUCAT1-binding protein involved in regulating splicing and processing of mRNAs. NR4A2 inhibits the inflammatory process driven by NF-κB. It was observed that cells lacking LUCAT1 expression had their splicing of immune genes altered, with reduced expression of NR4A2 (altered splicing on exon 7) in those cells lacking LUCAT1, as shown by ChIRP-MS assay in THP-1 cells.
Obesity and chronic inflammation in the liver trigger the most severe form of nonalcoholic fatty liver disease (NAFLD), steatohepatitis. Scientists at the University of Texas (UT) have shown how damaged hepatocytes accumulated in the liver after a vicious cycle of cytokine expression induced shedding of a critical liver receptor.
The controlled cell death process of apoptosis functions as the first step to any full recovery from injury or disease. In the second step of any recovery process, dead cells are cleared by efferocytosis, a process performed by phagocytotic cells like macrophages. Approximately 200-300 billion apoptotic cells are cleared daily by efferocytosis starting with the recognition of newly extracellular facing phosphatidylserine (PtdSer) by PtdSer-binding proteins present on phagocytotic cells.
Korean Research Institute of Bioscience and Biotechnology has described triterpenoid saponins isolated from Spinacia oleracea (spinach) reported to be useful for the treatment of inflammation.
The first in vivo cell atlas of senescent tissue in skeletal muscle has identified the damaging properties of these cells and explained why they block muscle regeneration. According to a study at Pompeu Fabra University led by scientists from Altos Labs Inc., cell damage caused the senescence of the cells, which secreted toxic substances into the surrounding microenvironment, causing fibrosis and preventing tissue regeneration.
Pharmablock Sciences (Nanjing) Inc. has divulged non-receptor tyrosine-protein kinase TYK2 inhibitors reported to be useful for the treatment of inflammation and autoimmune disease.
Unlike amphibians, mammals do not regenerate appendages. Except when they do. “If you amputate one of the branches off of the antler [of a reindeer], it will also regenerate,” Jeff Biernaskie told BioWorld. Even without amputation, the antlers of both male and female reindeer regenerate annually, including their skin. That regeneration is “the only large mammal model of true skin regeneration,” he said.
Liver damage arrests growth mediated by the somatotroph axis, which prevents liver cell death and inflammation, but increases fibrosis in nonalcoholic fatty liver disease (NAFLD). The explanation for this effect could lie in the relationship between the activating transcription factor 3 (ATF-3) and insulin-like growth factor 1 (IGF-1), according to a study from the University of California at Berkeley.
Retrotransposons could have a main role in the development of drug resistance in response to cancer treatment, according to a new study out of the Roswell Park Comprehensive Cancer Center. The transposition of DNA elements triggers an inflammatory response involved in the survival of cancer cells, a mechanism that could be blocked applying reverse transcriptase inhibitors, a class of drugs better known as anti-HIV medications.
Researchers from Eydis Bio Inc. reported the discovery and preclinical characterization of a novel mitogen-activated protein kinase kinase kinase 7 (MAP3K7/TAK1) inhibitor, EYD-001, being developed for the treatment of inflammatory and neuropathic pain.
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