G9P/CD158D Antibody
(Synonyms: CD158d, CD158D, KIR103AS, KIR2DL4, Killer cell immunoglobulin-like receptor 2DL4, CD158 antigen-like family member D, G9P, Killer cell inhibitory receptor 103AS, MHC class I NK cell receptor KIR103AS, KIR-103AS)G9P/CD158D Antibody (YA7099) is a Rabbit-derived and non-conjugated IgG polyclonal antibody, targeting to G9P/CD158D.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, FC
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Reactivity :
Human
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Formulation:
Supplied in PBS with 0.05% sodium azide
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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FC
FC: Flow Cytometry
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|---|---|---|---|
| Dilution Ratio | 1:1000-2000 | 1:100-500 | 1:20-50 |
Product Details
G9P/CD158D Antibody (YA7099) is a Rabbit-derived and non-conjugated IgG polyclonal antibody, targeting to G9P/CD158D.
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Host Mouse
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Clonality Polyclonal
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Species ReactivityHuman
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Calculated Molecular Weight Predicted band size: 41.5kDa;
SwissProt: SwissProt: Q99706
Purified recombinant fragment of human CD158D (AA: 290-330) expressed in E. Coli.
Endogenous
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS with 0.05% sodium azide
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
G9P/CD158D is a Receptor for non-classical major histocompatibility class Ib HLA-G molecules. Recognizes HLA-G in complex with B2M/beta-2 microglobulin and a nonamer self-peptide (peptide-bound HLA-G-B2M). In decidual NK cells, binds peptide-bound HLA-G-B2M complex and triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy. May play a role in balancing tolerance and antiviral-immunity at maternal-fetal interface by keeping in check the effector functions of NK, CD8+ T cells and B cells. Upon interaction with peptide-bound HLA-G-B2M, initiates signaling from the endosomal compartment leading to downstream activation of PRKDC-XRCC5 and AKT1, and ultimately triggering NF-kappa-B-dependent pro-inflammatory response[1][2][3][4][5].
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Subcellular Localization
Cell membrane; Early endosome membrane
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Expression
Tissue_Specificity: Expressed in decidual NK cells and innate lymphoid cell type I (ILC1). Expressed in a subset of peripheral NK cells. -
Isoforms & Post-Translational Modification
G9P/CD158D has 6 isoforms, Q99706-1: amino acid length is 377, molecular weight is 41487 Da (predicted); Q99706-2: amino acid length is 360, molecular weight is 39699 Da (predicted); Q99706-3: amino acid length is 342, molecular weight is 37356 Da (predicted); Q99706-4: amino acid length is 325, molecular weight is 35568 Da (predicted); Q99706-5: amino acid length is 307, molecular weight is 33591 Da (predicted); Q99706-6: amino acid length is 230, molecular weight is 24917 Da (predicted).
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Subunit
Interacts with peptide-bound HLA-G-B2M heterotrimeric complex.
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SwissProt ID
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Synonyms
CD158d, CD158D, KIR103AS, KIR2DL4, Killer cell immunoglobulin-like receptor 2DL4, CD158 antigen-like family member D, G9P, Killer cell inhibitory receptor 103AS, MHC class I NK cell receptor KIR103AS, KIR-103AS
Documentation
[1]. Rajagopalan S, et al. Activation of NK cells by an endocytosed receptor for soluble HLA-G. PLoS Biol. 2006 Jan;4(1):e9. [Content Brief]
[2]. Rajagopalan S, et al. Cellular senescence induced by CD158d reprograms natural killer cells to promote vascular remodeling. Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):20596-601. [Content Brief]
[3]. Fu B, et al. Natural Killer Cells Promote Fetal Development through the Secretion of Growth-Promoting Factors. Immunity. 2017 Dec 19;47(6):1100-1113.e6. [Content Brief]
[4]. Rajagopalan S, et al. A human histocompatibility leukocyte antigen (HLA)-G-specific receptor expressed on all natural killer cells. J Exp Med. 1999 Apr 5;189(7):1093-100. [Content Brief]
[5]. Rajagopalan S, et al. DNA-PKcs controls an endosomal signaling pathway for a proinflammatory response by natural killer cells. Sci Signal. 2010 Feb 23;3(110):ra14. [Content Brief]