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AB225660

Recombinant Human HLA G protein (His tag)

Recombinant Human HLA G protein (His tag)

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Recombinant Human HLA G protein (His tag) is a Human Full Length protein, in the 25 to 338 aa range, expressed in Mammalian, with >90%, suitable for SDS-PAGE, Mass Spec.

別名を表示する

HLA-6.0, HLAG, HLA-G, HLA G antigen, MHC class I antigen G

3 Images
Mass Spectrometry - Recombinant Human HLA G protein (His tag) (AB225660)
  • Mass Spec

Supplier Data

Mass Spectrometry - Recombinant Human HLA G protein (His tag) (AB225660)

Based on the SEQUEST from database of Mammalian Cell host and target protein, the LC-MS/MS Analysis result of ab225660 could indicate that this peptide derived from Mammalian Cell-expressed human HLA-G.

Mass Spectrometry - Recombinant Human HLA G protein (His tag) (AB225660)
  • Mass Spec

Supplier Data

Mass Spectrometry - Recombinant Human HLA G protein (His tag) (AB225660)

Based on the SEQUEST from database of Mammalian Cell host and target protein, the LC-MS/MS Analysis result of ab225660 could indicate that this peptide derived from Mammalian Cell-expressed human HLA-G.

SDS-PAGE - Recombinant Human HLA G protein (His tag) (AB225660)
  • SDS-PAGE

Supplier Data

SDS-PAGE - Recombinant Human HLA G protein (His tag) (AB225660)

(Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) analysis of ab225660 with 5% enrichment gel and 15% separation gel.

Key facts

精製度

>90% SDS-PAGE

発現系

Mammalian

タグ

6x His tag N-Terminus

アプリケーション

SDS-PAGE, Mass Spec

applications

生物活性

No

アクセッション番号

P17693

アニマルフリー

No

キャリアフリー

No

Human

バッファー組成

pH: 7.2 - 7.4 Constituents: Tris buffer, 50% Glycerol (glycerin, glycerine)

storage-buffer

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Reactivity", "Dilution Info", "Notes"] }, "values": { "SDS-PAGE": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" }, "Mass Spec": { "reactivity":"TESTED_AND_REACTS", "dilution-info":"", "notes":"<p></p>" } } }

配列情報

[{"linker":null,"sequence":"DAAQPARRAVRSLHHHHHHHHHHLVPRGSRTGSHSMRYFSAAVSRPGRGEPRFIAMGYVDDTQFVRFDSDSACPRMEPRAPWVEQEGPEYWEEETRNTKAHAQTDRMNLQTLRGYYNQSEASSHTLQWMIGCDLGSDGRLLRGYEQYAYDGKDYLALNEDLRSWTAADTAAQISKRKCEAANVAEQRRAYLEGTCVEWLHRYLENGKEMLQRADPPKTHVTHHPVFDYEATLRCWALGFYPAEIILTWQRDGEDQTQDVELVETRPAGDGTFQKWAAVVVPSGEEQRYTCHVQHEGLPEPLMLRWKQSSLPTIPIMGIVAGLVVLAAVVTGAAVAAVLWRKKSSD","proteinLength":"Full Length","predictedMolecularWeight":"39.6 kDa","actualMolecularWeight":null,"aminoAcidEnd":338,"aminoAcidStart":25,"nature":"Recombinant","expressionSystem":"Mammalian","accessionNumber":"P17693","tags":[{"tag":"6x His","terminus":"N-Terminus"}]}]

出荷温度及び保存条件

製品の状態
Liquid
出荷温度
Blue Ice
短期保存温度
-20°C
長期保存温度
-20°C
分注に関する情報
Upon delivery aliquot
保管に関する情報
Avoid freeze / thaw cycle
False

一般的な情報

機能

Isoform 1. Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed : 19304799, PubMed : 23184984, PubMed : 29262349). In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins (PubMed : 7584149, PubMed : 8805247). Peptide-bound HLA-G-B2M complex acts as a ligand for inhibitory/activating KIR2DL4, LILRB1 and LILRB2 receptors on uterine immune cells to promote fetal development while maintaining maternal-fetal tolerance (PubMed : 16366734, PubMed : 19304799, PubMed : 20448110, PubMed : 23184984, PubMed : 27859042, PubMed : 29262349). Upon interaction with KIR2DL4 and LILRB1 receptors on decidual NK cells, it triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy (PubMed : 16366734, PubMed : 19304799, PubMed : 23184984, PubMed : 29262349). Through interaction with KIR2DL4 receptor on decidual macrophages induces pro-inflammatory cytokine production mainly associated with tissue remodeling (PubMed : 19304799). Through interaction with LILRB2 receptor triggers differentiation of type 1 regulatory T cells and myeloid-derived suppressor cells, both of which actively maintain maternal-fetal tolerance (PubMed : 20448110, PubMed : 27859042). 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 (PubMed : 10190900, PubMed : 11290782, PubMed : 24453251). Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PubMed : 24453251). May induce immune activation/suppression via intercellular membrane transfer (trogocytosis), likely enabling interaction with KIR2DL4, which resides mostly in endosomes (PubMed : 20179272, PubMed : 26460007). Through interaction with the inhibitory receptor CD160 on endothelial cells may control angiogenesis in immune privileged sites (PubMed : 16809620).. Isoform 2. Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed : 11290782).. Isoform 3. Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed : 11290782).. Isoform 4. Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed : 11290782).. Isoform 5. Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed : 19304799, PubMed : 23184984, PubMed : 29262349). In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins (PubMed : 7584149, PubMed : 8805247). Peptide-bound HLA-G-B2M complex acts as a ligand for inhibitory/activating KIR2DL4, LILRB1 and LILRB2 receptors on uterine immune cells to promote fetal development while maintaining maternal-fetal tolerance (PubMed : 16366734, PubMed : 19304799, PubMed : 20448110, PubMed : 23184984, PubMed : 29262349). Upon interaction with KIR2DL4 and LILRB1 receptors on decidual NK cells, it triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy (PubMed : 16366734, PubMed : 19304799, PubMed : 23184984, PubMed : 29262349). Through interaction with KIR2DL4 receptor on decidual macrophages induces pro-inflammatory cytokine production mainly associated with tissue remodeling (PubMed : 19304799). Through interaction with LILRB2 receptor triggers differentiation of type 1 regulatory T cells and myeloid-derived suppressor cells, both of which actively maintain maternal-fetal tolerance (PubMed : 20448110). Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PubMed : 24453251).. Isoform 6. Likely does not bind B2M and presents peptides.. Isoform 7. Likely does not bind B2M and presents peptides.

配列の類似性

Belongs to the MHC class I family.

翻訳後修飾

N-glycosylated.. Soluble HLA class I histocompatibility antigen, alpha chain G. Produced by proteolytic cleavage at the cell surface (shedding) by matrix metalloproteinase MMP2.

製品プロトコール

ターゲットの情報

Isoform 1. Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed : 19304799, PubMed : 23184984, PubMed : 29262349). In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins (PubMed : 7584149, PubMed : 8805247). Peptide-bound HLA-G-B2M complex acts as a ligand for inhibitory/activating KIR2DL4, LILRB1 and LILRB2 receptors on uterine immune cells to promote fetal development while maintaining maternal-fetal tolerance (PubMed : 16366734, PubMed : 19304799, PubMed : 20448110, PubMed : 23184984, PubMed : 27859042, PubMed : 29262349). Upon interaction with KIR2DL4 and LILRB1 receptors on decidual NK cells, it triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy (PubMed : 16366734, PubMed : 19304799, PubMed : 23184984, PubMed : 29262349). Through interaction with KIR2DL4 receptor on decidual macrophages induces pro-inflammatory cytokine production mainly associated with tissue remodeling (PubMed : 19304799). Through interaction with LILRB2 receptor triggers differentiation of type 1 regulatory T cells and myeloid-derived suppressor cells, both of which actively maintain maternal-fetal tolerance (PubMed : 20448110, PubMed : 27859042). 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 (PubMed : 10190900, PubMed : 11290782, PubMed : 24453251). Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PubMed : 24453251). May induce immune activation/suppression via intercellular membrane transfer (trogocytosis), likely enabling interaction with KIR2DL4, which resides mostly in endosomes (PubMed : 20179272, PubMed : 26460007). Through interaction with the inhibitory receptor CD160 on endothelial cells may control angiogenesis in immune privileged sites (PubMed : 16809620).. Isoform 2. Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed : 11290782).. Isoform 3. Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed : 11290782).. Isoform 4. Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed : 11290782).. Isoform 5. Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed : 19304799, PubMed : 23184984, PubMed : 29262349). In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins (PubMed : 7584149, PubMed : 8805247). Peptide-bound HLA-G-B2M complex acts as a ligand for inhibitory/activating KIR2DL4, LILRB1 and LILRB2 receptors on uterine immune cells to promote fetal development while maintaining maternal-fetal tolerance (PubMed : 16366734, PubMed : 19304799, PubMed : 20448110, PubMed : 23184984, PubMed : 29262349). Upon interaction with KIR2DL4 and LILRB1 receptors on decidual NK cells, it triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy (PubMed : 16366734, PubMed : 19304799, PubMed : 23184984, PubMed : 29262349). Through interaction with KIR2DL4 receptor on decidual macrophages induces pro-inflammatory cytokine production mainly associated with tissue remodeling (PubMed : 19304799). Through interaction with LILRB2 receptor triggers differentiation of type 1 regulatory T cells and myeloid-derived suppressor cells, both of which actively maintain maternal-fetal tolerance (PubMed : 20448110). Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PubMed : 24453251).. Isoform 6. Likely does not bind B2M and presents peptides.. Isoform 7. Likely does not bind B2M and presents peptides.
See full target information HLA-G

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