SLAMF6 Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 实验流程
- 背景知识
Application ![]()
| WB, E |
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Primary Accession | Q96DU3 |
Other Accession | NP_443163.1, NP_001171644.1 |
Reactivity | Human |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 37345 Da |
Antigen Region | 277-305 aa |
Gene ID | 114836 |
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Other Names | SLAM family member 6, Activating NK receptor, NK-T-B-antigen, NTB-A, CD352, SLAMF6, KALI |
Target/Specificity | This SLAMF6 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 277-305 amino acids from the C-terminal region of human SLAMF6. |
Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain 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. |
Precautions | SLAMF6 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | SLAMF6 |
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Synonyms | KALI |
Function | Self-ligand receptor of the signaling lymphocytic activation molecule (SLAM) family. SLAM receptors triggered by homo- or heterotypic cell-cell interactions are modulating the activation and differentiation of a wide variety of immune cells and thus are involved in the regulation and interconnection of both innate and adaptive immune response. Activities are controlled by presence or absence of small cytoplasmic adapter proteins, SH2D1A/SAP and/or SH2D1B/EAT-2. Triggers cytolytic activity only in natural killer cells (NK) expressing high surface densities of natural cytotoxicity receptors (PubMed:11489943, PubMed:16920955). Positive signaling in NK cells implicates phosphorylation of VAV1. NK cell activation seems to depend on SH2D1B and not on SH2D1A (PubMed:16920955). In conjunction with SLAMF1 controls the transition between positive selection and the subsequent expansion and differentiation of the thymocytic natural killer T (NKT) cell lineage (By similarity). Promotes T-cell differentiation into a helper T-cell Th17 phenotype leading to increased IL-17 secretion; the costimulatory activity requires SH2D1A (PubMed:16920955, PubMed:22184727). Promotes recruitment of RORC to the IL-17 promoter (PubMed:22989874). In conjunction with SLAMF1 and CD84/SLAMF5 may be a negative regulator of the humoral immune response. In the absence of SH2D1A/SAP can transmit negative signals to CD4(+) T- cells and NKT cells. Negatively regulates germinal center formation by inhibiting T-cell:B-cell adhesion; the function probably implicates increased association with PTPN6/SHP-1 via ITSMs in absence of SH2D1A/SAP. However, reported to be involved in maintaining B-cell tolerance in germinal centers and in preventing autoimmunity (By similarity). |
Cellular Location | Cell membrane; Single-pass type I membrane protein |
Tissue Location | Expressed by all (resting and activated) natural killer cells (NK), T- and B-lymphocytes (PubMed:11489943). Increased surface expression on T-cells of systemic lupus erythematosus (SLE) patients (PubMed:22184727). |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The protein encoded by this gene is a type I transmembrane protein, belonging to the CD2 subfamily of the immunoglobulin superfamily. This encoded protein is expressed on Natural killer (NK), T, and B lymphocytes. It undergoes tyrosine phosphorylation and associates with the Src homology 2 domain-containing protein (SH2D1A) as well as with SH2 domain-containing phosphatases (SHPs). It functions as a coreceptor in the process of NK cell activation. It can also mediate inhibitory signals in NK cells from X-linked lymphoproliferative patients. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
REFERENCES
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)
Rose, J.E., et al. Mol. Med. 16 (7-8), 247-253 (2010) :
Davila, S., et al. Genes Immun. 11(3):232-238(2010)
Need, A.C., et al. Hum. Mol. Genet. 18(23):4650-4661(2009)
Talmud, P.J., et al. Am. J. Hum. Genet. 85(5):628-642(2009)

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