SIRPα (CD172a) #
Alternative names: SIRPA, SHPS-1, BIT, MFR, MYD-1, P84, SHPS-1, SHPS1, SIRP
In humans and in mice, SIRPα can be found on the surface of: dendritic cells, granulocytes, macrophages/monocytes, stem cells/precursors
Ligands: CD47, PTPN11
Associated molecules: SHP-2
Function: signal transduction, cell adhesion, macrophage fusion
Additional information: SIRPα is also known as CD172a. CD172a is a negative regulator of downstream kinase signaling cascades and binds to CD47 (the “don’t eat me” signal). By associating with SHP-2 after CD47 binding, CD172a negatively regulates the downstream signal pathways controlled by epidermal growth factor, thus reducing cell growth, migration, and transformation. CD172a is critical to preventing phagocytosis of self, promoting self-tolerance. CD172a is also involved in macrophage fusion, which leads to the formation of giant cells. CD47 binding prevents maturation of immature dendritic cells and inhibits cytokine production by mature dendritic cells. In various cancer types, CD172a expression is downregulated.
A macromolecular complex of 5 small nuclear RNAs (snRNAs) and approximately 100 proteins that removes introns from precursor RNAs and joins the remaining exon sections to generate an mRNA. The spliceosome forms on a gene's primary RNA transcript, catalyzing the splicing process as the gene is transcribed. The snRNAs are critical for recognizing specific sites in the pre-mRNA and for catalyzing the process. Each of the snRNAs binds one or more of a set of specific proteins known as splicing factors, which are the protein components of the spliceosome. Transcription and splicing occur concurrently in mammalian cells, suggesting potential regulatory interactions.