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>   首页   >   产品   >   一抗   >   其他   >   SIGLEC10 Antibody (C-term)   

SIGLEC10 Antibody (C-term) 精选

Affinity Purified Rabbit Polyclonal Antibody (Pab)

     
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, E
Primary Accession Q96LC7
Other Accession NP_001164628.1, NP_001164627.1
Reactivity Human
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 76592 Da
Antigen Region 667-695 aa
Additional Information
Gene ID 89790
Other Names Sialic acid-binding Ig-like lectin 10, Siglec-10, Siglec-like protein 2, SIGLEC10, SLG2
Target/Specificity This SIGLEC10 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 667-695 amino acids from the C-terminal region of human SIGLEC10.
Dilution WB~~1:1000
E~~Use at an assay dependent concentration.
Format Purified polyclonal antibody supplied in PBS with 0.05% (V/V) Proclin 300. This antibody is purified through a protein A column, followed by peptide affinity purification.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsSIGLEC10 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.

For Research Use Only. Not For Use In Diagnostic Procedures.

Protein Information
Name SIGLEC10
Synonyms SLG2
Function Putative adhesion molecule that mediates sialic-acid dependent binding to cells. Preferentially binds to alpha-2,3- or alpha-2,6-linked sialic acid (By similarity). The sialic acid recognition site may be masked by cis interactions with sialic acids on the same cell surface. In the immune response, seems to act as an inhibitory receptor upon ligand induced tyrosine phosphorylation by recruiting cytoplasmic phosphatase(s) via their SH2 domain(s) that block signal transduction through dephosphorylation of signaling molecules (PubMed:11284738, PubMed:12163025). Involved in negative regulation of B-cell antigen receptor signaling. The inhibition of B cell activation is dependent on PTPN6/SHP-1 (By similarity). In association with CD24 may be involved in the selective suppression of the immune response to danger-associated molecular patterns (DAMPs) such as HMGB1, HSP70 and HSP90 (By similarity). In association with CD24 may regulate the immune repsonse of natural killer (NK) cells (PubMed:25450598). Plays a role in the control of autoimmunity (By similarity). During initiation of adaptive immune responses by CD8- alpha(+) dendritic cells inhibits cross-presentation by impairing the formation of MHC class I-peptide complexes. The function seems to implicate recruitment of PTPN6/SHP-1, which dephosphorylates NCF1 of the NADPH oxidase complex consequently promoting phagosomal acidification (By similarity).
Cellular Location [Isoform 1]: Cell membrane; Single-pass type I membrane protein [Isoform 3]: Cell membrane; Single-pass type I membrane protein [Isoform 5]: Secreted.
Tissue Location Expressed by peripheral blood leukocytes (eosinophils, monocytes and a natural killer cell subpopulation) Isoform 5 is found to be the most abundant isoform. Found in lymph node, lung, ovary and appendix. Isoform 1 is found at high levels and isoform 2 at lower levels in bone marrow, spleen and spinal cord Isoform 2 is also found in brain. Isoform 4 is specifically found in natural killer cells.
Research Areas

BACKGROUND

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).

REFERENCES

Davila, S., et al. Genes Immun. 11(3):232-238(2010)
Kivi, E., et al. Blood 114(26):5385-5392(2009)
Szafranski, K., et al. Genome Biol. 8 (8), R154 (2007) :
Clark, H.F., et al. Genome Res. 13(10):2265-2270(2003)
Kitzig, F., et al. Biochem. Biophys. Res. Commun. 296(2):355-362(2002)

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