产品: KLRK1 抗体
货号: DF4816
描述: Rabbit polyclonal antibody to KLRK1
应用: WB IHC IF/ICC
反应: Human, Mouse
分子量: 25 KD; 25kD(Calculated).
蛋白号: P26718
RRID: AB_2837167

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 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

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产品描述

来源:
Rabbit
应用:
IHC 1:50-1:200, WB 1:500-1:1000, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human,Mouse
克隆:
Polyclonal
特异性:
KLRK1 Antibody detects endogenous levels of total KLRK1.
RRID:
AB_2837167
引用格式: Affinity Biosciences Cat# DF4816, RRID:AB_2837167.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

CD314; CD314 antigen; D12S2489E; Killer cell lectin like receptor subfamily K member 1; Killer cell lectin-like receptor subfamily K member 1; KLR; KLRC4 KLRK1 readthrough; KLRK1; NK cell receptor D; NK lectin-like receptor; NKG2 D activating NK receptor; NKG2 D type II integral membrane protein; NKG2-D; NKG2-D type II integral membrane protein; NKG2-D-activating NK receptor; Nkg2d; NKG2D_HUMAN; NKLLR; NKR P2; Nkrp2;

抗原和靶标

免疫原:
Uniprot:
基因/基因ID:
表达:
P26718 NKG2D_HUMAN:

Expressed in natural killer (NK) cells, CD8(+) alpha-beta and gamma-delta T-cells. Expressed on essentially all CD56+CD3- NK cells from freshly isolated PBMC. Expressed in interferon-producing killer dendritic cells (IKDCs).

序列:
MGWIRGRRSRHSWEMSEFHNYNLDLKKSDFSTRWQKQRCPVVKSKCRENASPFFFCCFIAVAMGIRFIIMVAIWSAVFLNSLFNQEVQIPLTESYCGPCPKNWICYKNNCYQFFDESKNWYESQASCMSQNASLLKVYSKEDQDLLKLVKSYHWMGLVHIPTNGSWQWEDGSILSPNLLTIIEMQKGDCALYASSFKGYIENCSTPNTYICMQRTV

翻译修饰 - P26718 作为底物

Site PTM Type Enzyme
S9 Phosphorylation
S12 Phosphorylation
S16 Phosphorylation
T205 Phosphorylation
Y209 Phosphorylation

研究背景

功能:

Functions as an activating and costimulatory receptor involved in immunosurveillance upon binding to various cellular stress-inducible ligands displayed at the surface of autologous tumor cells and virus-infected cells. Provides both stimulatory and costimulatory innate immune responses on activated killer (NK) cells, leading to cytotoxic activity. Acts as a costimulatory receptor for T-cell receptor (TCR) in CD8(+) T-cell-mediated adaptive immune responses by amplifying T-cell activation. Stimulates perforin-mediated elimination of ligand-expressing tumor cells. Signaling involves calcium influx, culminating in the expression of TNF-alpha. Participates in NK cell-mediated bone marrow graft rejection. May play a regulatory role in differentiation and survival of NK cells. Binds to ligands belonging to various subfamilies of MHC class I-related glycoproteins including MICA, MICB, RAET1E, RAET1G, RAET1L/ULBP6, ULBP1, ULBP2, ULBP3 (ULBP2>ULBP1>ULBP3) and ULBP4.

细胞定位:

Cell membrane>Single-pass type II membrane protein.
Note: Colocalized with HCST on the cell surface.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
组织特异性:

Expressed in natural killer (NK) cells, CD8(+) alpha-beta and gamma-delta T-cells. Expressed on essentially all CD56+CD3- NK cells from freshly isolated PBMC. Expressed in interferon-producing killer dendritic cells (IKDCs).

亚基结构:

Homodimer; disulfide-linked. Heterohexamer composed of two subunits of KLRK1 and four subunits of HCST/DAP10. Interacts (via transmembrane domain) with HCST/DAP10 (via transmembrane domain); the interaction is required for KLRK1 NK cell surface and induces NK cell-mediated cytotoxicity. Does not interact with TYROBP. Interacts with CEACAM1; recruits PTPN6 that dephosphorylates VAV1.

研究领域

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Organismal Systems > Immune system > Natural killer cell mediated cytotoxicity.   (View pathway)

文献引用

1). CircARAP2 controls sMICA-induced NK cell desensitization by erasing CTCF/PRC2-induced suppression in early endosome marker RAB5A. Cellular and molecular life sciences : CMLS, 2024 (PubMed: 39048814) [IF=8.0]

Application: WB    Species: Human    Sample: NK cell

Fig. 1 CircARAP2 is upregulated in sMICA-induced NK cell desensitization. A The workflow of profiling circRNAs associated with sMICA-induced NK cell desensitization. B Flow cytometry and RT-qPCR analysis of NKG2D expression on NK92 and human primary activated NK cells treated with rsMICA for 24 h. n = 3 for NK92 cells, n = 8 for activated NK cells; Unpaired two-tailed t-test for RT-qPCR analysis, paired two-tailed t-test for flow cytometry analysis. C Left panel, Representative IF image of NKG2D and RAB5 on NK92 (Scale bar, 20 μm) and human primary activated NK (Scale bar, 10 μm) cells treated with rsMICA; Right panel, Quantification of Pearson coefficient of colocalization in pairs NKG2D/RAB5 on NK92 and human primary activated NK cells following rsMICA treatment (Repeats = 3, unpaired two-tailed t-test). D Immunoblot of NKG2D in both NK92 and human primary activated NK cells treated with rsMICA. Data represent three independent experiments, unpaired two-tailed t-test. E The calcein-AM release assay was used to assess the cytotoxicity of NK92 and human primary activated NK cells following rsMICA treatment. Data are presented of three independent experiments, two-way ANOVA. F Flow cytometry was used to assess the IFN-γ, Granzyme B and CD107a expression in both NK92 and human primary activated NK cells treated with rsMICA. Data are presented of three independent experiments, paired two-tailed t-test. G Flow cytometry was used to assess the expression of inhibitory receptors TIGIT and CD96 in NK92 and human primary activated NK cells with rsMICA treatment. Data are presented of three independent experiments, paired two-tailed t-test. H Volcano plot showing differentially expressed circRNAs in NK92 samples with or without rsMICA treatment (Left panel). KEGG analysis showing enrichment of differentially expressed circRNAs in the endocytosis pathway (Middle panel). Heatmap showing changes in expression levels of circRNAs enriched in the endocytosis pathway (Right panel). I Expression of circARAP2 and linear ARAP2 in both NK92 (n = 3) and primary activated NK cells (n = 10) after treatment with rsMICA. Unpaired two-tailed t-test was used for the comparison of two groups. (ns no significance, *P 

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