(1)
(5)
产品描述
来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:
*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, Rat
克隆:
Polyclonal
特异性:
COPS5 Antibody detects endogenous levels of total COPS5.
RRID:
AB_2838564
引用格式: Affinity Biosciences Cat# DF6602, RRID:AB_2838564.
引用格式: Affinity Biosciences Cat# DF6602, RRID:AB_2838564.
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
38 kDa Mov34 homolog; COP9 (constitutive photomorphogenic) homolog subunit 5; COP9 constitutive photomorphogenic homolog subunit 5; COP9 signalosome complex subunit 5; COP9 signalosome subunit 5; Cop9 subunit 5; COPS 5; cops5; CSN 5; CSN5; CSN5_HUMAN; JAB 1; Jun activation domain binding protein 1; Jun activation domain binding protein; Jun activation domain-binding protein 1; MGC3149; MOV 34; MOV34; MOV34 family, 38-KD member; SGN 5; SGN5; Signalosome subunit 5;
抗原和靶标
免疫原:
A synthesized peptide derived from human COPS5, corresponding to a region within the internal amino acids.
基因/基因ID:
描述:
The COP9 Signalosome (CSN) is a ubiquitously expressed multiprotein complex that is involved in a vast array of cellular and developmental processes, which is thought to be attributed to its control over the ubiquitin-proteasome pathway. Typically, the CSN is composed of eight highly conserved subunits (CSN1-CSN8), each of which is homologous to one of the eight subunits that form the lid of the 26S proteasome particle, suggesting that these complexes have a common evolutionary ancestor (1). CSN was first identified in Arabidopsis thaliana mutants with a light-grown seedling phenotype when grown in the dark (2-4). The subsequent cloning of the constitutive morphogenesis 9 (cop9) mutant from Arabidopsis thaliana was soon followed by the biochemical purification of the COP9-containing multiprotein complex (4). It is now widely accepted that the CSN directly interacts with cullin-RING ligase (CRL) families of ubiquitin E3 complexes, and that CSN is required for their proper function (5). In addition, CSN may also regulate protein homeostasis through its association with protein kinases and deubiquitinating enzymes. Collectively, these activities position the CSN as a pivotal regulator of the DNA-damage response, cell-cycle control, and gene expression (1). COPS5/CSN5/Jab1 (c-Jun activation domain-binding protein-1) was originally identified as a transcriptional coactivator of c-Jun and subsequently discovered to be a fifth component and integral part of the CSN (6). As the catalytic center of the CSN, COPS5 is able to integrate multiple functions of the CSN complex such as cell-cycle control, transcription, and DNA-damage response by regulating the activity of CRLs through deneddylation of cullins (7).
文献引用
1). Calcium Channel Blocker Nifedipine Suppresses Colorectal Cancer Progression and Immune Escape by Preventing NFAT2 Nuclear Translocation. , 2020
Application: WB Species: Human Sample: SW620 cells
Figure 5. NFAT2 Recruits Phosphorylated STAT3 to Elevate the Expression of Downstream Effectors (A) The colocalization of p-STAT3 (green) and NFAT2 (red) in control and LASP1-overexpressing SW620 cells was assessed by IF staining. The scale bar represents 50 mm. (B) Analysis of the correlation between NFAT2 and p-STAT3 in clinical tissues with high and low expression of NFAT2 by IHC staining. The right panel presents the percentage of patients with high or low expression of CRC tissue. Scale bar represents 50 mm. (C) Endogenous interaction between NFAT2 and p-STAT3 in control and LASP1-overexpressing SW620 cells. (D) Endogenous interaction between NFAT2 and p-STAT3 in SW620 cells after treatment with NIFE or BAY was detected by coIP assays. (E) The transcriptional regulation of the downstream genes COPS5, TWIST1, MMP2, and PD-L1 by NFAT2 and p-STAT3 was detected by ChIP assays. (F) The binding sites between NFAT2 and the downstream genes were confirmed by a dual-luciferase reporter system. (G) Left panel: the expression of NFAT2 and downstream genes in control and NIFE-treated SW620 cells were detected by qPCR. Right panel: the expression alterations in downstream genes in the indicated cells treated with NIFE or BAY were detected by WB. (H) The relationship between NFAT2 and downstream genes was detected from the GEO database. (I) IHC analysis was performed to detect the expression of NFAT2, TWIST1, COPS5, and MMP2 in human CRC tissues. Two representative cases are shown. Percentage of patients with high or low expression of CRC tissue on the right panel. Scale bar represents 50 mm. (G) After treating SW620 cells with CsA (10 mM), VIVIT (10 mM), and FK506 (10 ng/mL) and subsequently separating the nuclear and cytoplasmic proteins, WB analysis was used to detect the level of NFAT2 in the nucleus and p-NFAT2 in the cytoplasm. (H) Representative images of IHC staining analysis of NFAT2 expression in CRC tissues and adjacent nontumor tissues. The bar chart on the right represents the percentage of high and low NFAT2 expression cases in normal and CRC tissues. (I) IHC analysis of NFAT2 and p-NFAT2 expression in nonmetastatic and metastatic CRC tissues. The bar chart on the right represents the percentage of high and low NFAT2 or p-NFAT2 expression cases in nonmetastatic CRC and metastatic CRC tissues.
Application: IHC Species: Human Sample: SW620 cells
Figure 5. NFAT2 Recruits Phosphorylated STAT3 to Elevate the Expression of Downstream Effectors (A) The colocalization of p-STAT3 (green) and NFAT2 (red) in control and LASP1-overexpressing SW620 cells was assessed by IF staining. The scale bar represents 50 mm. (B) Analysis of the correlation between NFAT2 and p-STAT3 in clinical tissues with high and low expression of NFAT2 by IHC staining. The right panel presents the percentage of patients with high or low expression of CRC tissue. Scale bar represents 50 mm. (C) Endogenous interaction between NFAT2 and p-STAT3 in control and LASP1-overexpressing SW620 cells. (D) Endogenous interaction between NFAT2 and p-STAT3 in SW620 cells after treatment with NIFE or BAY was detected by coIP assays. (E) The transcriptional regulation of the downstream genes COPS5, TWIST1, MMP2, and PD-L1 by NFAT2 and p-STAT3 was detected by ChIP assays. (F) The binding sites between NFAT2 and the downstream genes were confirmed by a dual-luciferase reporter system. (G) Left panel: the expression of NFAT2 and downstream genes in control and NIFE-treated SW620 cells were detected by qPCR. Right panel: the expression alterations in downstream genes in the indicated cells treated with NIFE or BAY were detected by WB. (H) The relationship between NFAT2 and downstream genes was detected from the GEO database. (I) IHC analysis was performed to detect the expression of NFAT2, TWIST1, COPS5, and MMP2 in human CRC tissues. Two representative cases are shown. Percentage of patients with high or low expression of CRC tissue on the right panel. Scale bar represents 50 mm. (G) After treating SW620 cells with CsA (10 mM), VIVIT (10 mM), and FK506 (10 ng/mL) and subsequently separating the nuclear and cytoplasmic proteins, WB analysis was used to detect the level of NFAT2 in the nucleus and p-NFAT2 in the cytoplasm. (H) Representative images of IHC staining analysis of NFAT2 expression in CRC tissues and adjacent nontumor tissues. The bar chart on the right represents the percentage of high and low NFAT2 expression cases in normal and CRC tissues. (I) IHC analysis of NFAT2 and p-NFAT2 expression in nonmetastatic and metastatic CRC tissues. The bar chart on the right represents the percentage of high and low NFAT2 or p-NFAT2 expression cases in nonmetastatic CRC and metastatic CRC tissues.
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