SIGLEC10
Sialic acid-binding Ig-like lectin 10 is a protein that in humans is encoded by the SIGLEC10 gene.[1][2] The mouse orthologue is Siglec G.
Structure and Function
Structure and Function
Like most but not all other Siglecs, Siglec-10 bears an ITIM (Immunoreceptor tyrosine-based inhibitory motif) within its cytoplasmic domain. Siglec-10 is a ligand for CD52, the target of the therapeutic monoclonal antibody Alemtuzumab.[3] It is also reported to bind to Vascular adhesion protein 1 (VAP-1) and to the co-stimulatory molecule CD24 also known as HSA (Heat-stable antigen).
Gene Family summary
Gene Family summary
SIGLECs are members of the immunoglobulin superfamily that are expressed on the cell surface. Most SIGLECs have 1 or more cytoplasmic immune receptor tyrosine-based inhibitory motifs, or ITIMs. SIGLECs are typically expressed on cells of the innate immune system, with the exception of the B-cell expressed SIGLEC6 (MIM 604405).[supplied by OMIM][2]
References
References
- ↑ Munday J, Kerr S, Ni J, Cornish AL, Zhang JQ, Nicoll G, Floyd H, Mattei MG, Moore P, Liu D, Crocker PR (Apr 2001). “Identification, characterization and leucocyte expression of Siglec-10, a novel human sialic acid-binding receptor”. Biochem J. 355 (Pt 2): 489–97. doi:10.1042/0264-6021:3550489. PMC 1221762. PMID 11284738.
- ↑ 2.0 2.1 “Entrez Gene: SIGLEC10 sialic acid binding Ig-like lectin 10”.
- ↑ Clark, M. & A. Cooke (2013). “Regulation unmasked by activation”. Nat Immunol. 14: 696–697. doi:10.1038/ni.2646.
Further reading
Further reading
- Li N, Zhang W, Wan T, et al. (2001). “Cloning and characterization of Siglec-10, a novel sialic acid binding member of the Ig superfamily, from human dendritic cells”. J. Biol. Chem. 276 (30): 28106–12. doi:10.1074/jbc.M100467200. PMID 11358961.
- Yousef GM, Ordon MH, Foussias G, Diamandis EP (2001). “Molecular characterization, tissue expression, and mapping of a novel Siglec-like gene (SLG2) with three splice variants”. Biochem. Biophys. Res. Commun. 284 (4): 900–10. doi:10.1006/bbrc.2001.5053. PMID 11409878.
- Nagano T, Yoneda T, Hatanaka Y, et al. (2002). “Filamin A-interacting protein (FILIP) regulates cortical cell migration out of the ventricular zone”. Nat. Cell Biol. 4 (7): 495–501. doi:10.1038/ncb808. PMID 12055638.
- Kitzig F, Martinez-Barriocanal A, López-Botet M, Sayós J (2002). “Cloning of two new splice variants of Siglec-10 and mapping of the interaction between Siglec-10 and SHP-1”. Biochem. Biophys. Res. Commun. 296 (2): 355–62. doi:10.1016/S0006-291X(02)00885-9. PMID 12163025.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2003). “Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences”. Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
- Clark HF, Gurney AL, Abaya E, et al. (2003). “The secreted protein discovery initiative (SPDI), a large-scale effort to identify novel human secreted and transmembrane proteins: a bioinformatics assessment”. Genome Res. 13 (10): 2265–70. doi:10.1101/gr.1293003. PMC 403697. PMID 12975309.
- Gerhard DS, Wagner L, Feingold EA, et al. (2004). “The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC)”. Genome Res. 14 (10B): 2121–7. doi:10.1101/gr.2596504. PMC 528928. PMID 15489334.
- Kimura K, Wakamatsu A, Suzuki Y, et al. (2006). “Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes”. Genome Res. 16 (1): 55–65. doi:10.1101/gr.4039406. PMC 1356129. PMID 16344560.
- Szafranski K, Schindler S, Taudien S, et al. (2007). “Violating the splicing rules: TG dinucleotides function as alternative 3′ splice sites in U2-dependent introns”. Genome Biol. 8 (8): R154. doi:10.1186/gb-2007-8-8-r154. PMC 2374985. PMID 17672918.
Looking for the patient version?
© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH