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Rabbit Anti-GPS1/Cy7 Conjugated antibody (bs-9126R-Cy7)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bs-9126R-Cy7
英文名稱1 Rabbit Anti-GPS1/Cy7 Conjugated antibody
中文名稱 Cy7標(biāo)記的G蛋白通路抑制蛋白1抗體
別    名 Arabidopsis Fus6/Cop 11 homolog; Arabidopsis Fus6/Cop 11 homolog; constitutive photomorphogenic homolog subunit 1; constitutive photomorphogenic homolog subunit 1; COP9; COP9 signalosome complex subunit 1; COP9 signalosome complex subunit 1; COPS1; COPS1; CSN 1; CSN1_HUMAN; G protein pathway suppressor 1; G protein pathway suppressor 1; GPS-1; GPS1; GPS1; JAB1-containing signalosome subunit 1; MFH protein; MFH protein; Protein GPS1; Protein MFH; SGN1; Signalosome subunit 1; Y59A8A.1.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領(lǐng)域 細(xì)胞生物  免疫學(xué)  神經(jīng)生物學(xué)  信號轉(zhuǎn)導(dǎo)  激酶和磷酸酶  G蛋白信號  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) (predicted: Human, Mouse, Rat, Chicken, Dog, Cow, )
產(chǎn)品應(yīng)用
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 55kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human GPS1/CSN1
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產(chǎn)品介紹 background:
Essential component of the COP9 signalosome complex (CSN), a complex involved in various cellular and developmental processes. The CSN complex is an essential regulator of the ubiquitin (Ubl) conjugation pathway by mediating the deneddylation of the cullin subunits of SCF-type E3 ligase complexes, leading to decrease the Ubl ligase activity of SCF-type complexes such as SCF, CSA or DDB2. The complex is also involved in phosphorylation of p53/TP53, c-jun/JUN, IkappaBalpha/NFKBIA, ITPK1 and IRF8/ICSBP, possibly via its association with CK2 and PKD kinases. CSN-dependent phosphorylation of TP53 and JUN promotes and protects degradation by the Ubl system, respectively. Suppresses G-protein-and mitogen-activated protein kinase-mediated signal transduction.

Function:
Essential component of the COP9 signalosome complex (CSN), a complex involved in various cellular and developmental processes. The CSN complex is an essential regulator of the ubiquitin (Ubl) conjugation pathway by mediating the deneddylation of the cullin subunits of SCF-type E3 ligase complexes, leading to decrease the Ubl ligase activity of SCF-type complexes such as SCF, CSA or DDB2. The complex is also involved in phosphorylation of p53/TP53, c-jun/JUN, IkappaBalpha/NFKBIA, ITPK1 and IRF8/ICSBP, possibly via its association with CK2 and PKD kinases. CSN-dependent phosphorylation of TP53 and JUN promotes and protects degradation by the Ubl system, respectively. Suppresses G-protein-and mitogen-activated protein kinase-mediated signal transduction.

Subunit:
Component of the CSN complex, composed of COPS1/GPS1, COPS2, COPS3, COPS4, COPS5, COP6, COPS7 (COPS7A or COPS7B) and COPS8. In the complex, it probably interacts directly with COPS2, COPS3, COPS4 and CSN5. Interacts directly with inositol kinase ITPK1. Interacts with CAPN8 (By similarity).

Subcellular Location:
Cytoplasm. Nucleus.

Tissue Specificity:
Widely expressed.

Post-translational modifications:
Phosphorylated upon DNA damage, probably by ATM or ATR.

Similarity:
Belongs to the CSN1 family.
Contains 1 PCI domain.

Database links:

Entrez Gene: 2873 Human

Entrez Gene: 209318 Mouse

Entrez Gene: 117039 Rat

Omim: 601934 Human

SwissProt: Q13098 Human

SwissProt: Q99LD4 Mouse

SwissProt: P97834 Rat

Unigene: 268530 Human

Unigene: 30195 Mouse

Unigene: 16873 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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