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Systemic scleroderma, or systemic sclerosis, is an autoimmune rheumatic disease characterised by excessive production and accumulation of collagen, called fibrosis, in the skin and internal organs and by injuries to small arteries. There are two major subgroups of systemic sclerosis based on the extent of skin involvement: limited and diffuse ...
5739 19222 Ensembl ENSG00000160013 ENSMUSG00000043017 UniProt P43119 P43252 RefSeq (mRNA) NM_000960 NM_008967 RefSeq (protein) NP_000951 NP_032993 Location (UCSC) Chr 19: 46.62 – 46.63 Mb Chr 7: 16.64 – 16.64 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse The prostacyclin receptor, also termed the prostaglandin I 2 receptor or just IP, is a receptor belonging to the ...
Since this activity occurs in the nucleus of the cell ATA is a form of antinuclear antibody. Scleroderma results from the overproduction of collagen in affected tissues, one study claims that there is an increased density of Topoisomerase I sites in the collagen genes, and that the antibodies may be altering transcription at these loci. [7]
Primary lateral sclerosis, progressive muscle weakness in the voluntary muscles. Primary sclerosing cholangitis, a hardening of the bile duct by scarring and repeated inflammation. Systemic sclerosis (progressive systemic scleroderma), a rare, chronic disease which affects the skin, and in some cases also blood vessels and internal organs.
In cell biology, there are a multitude of signalling pathways. Cell signalling is part of the molecular biology system that controls and coordinates the actions of cells.. Akt/PKB signalling pathway
T-cell–B-cell discordance – A normal immune response is assumed to involve B and T cell responses to the same antigen, even if we know that B cells and T cells recognise very different things: conformations on the surface of a molecule for B cells and pre-processed peptide fragments of proteins for T cells. However, there is nothing as far ...
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Many of the cytokines elevated in CRS are not produced by CAR-T cells, but by myeloid cells that are pathogenically licensed through T-cell-mediated activating mechanisms. For example, in vitro co-culture experiments have demonstrated IL-6, MCP-1, and MIP-1 are not produced by CAR-T cells, but rather by inflammatory myeloid lineage cells. [ 13 ]