COPS5 Antibody - #DF6602

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Product: COPS5 Antibody
Catalog: DF6602
Description: Rabbit polyclonal antibody to COPS5
Application: WB IHC IF/ICC
Cited expt.: WB, IHC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 37kDa; 38kD(Calculated).
Uniprot: Q92905
RRID: AB_2838564

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 100ul $280 In stock
 200ul $350 In stock

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Related Downloads
MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
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:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Zebrafish(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
COPS5 Antibody detects endogenous levels of total COPS5.
RRID:
AB_2838564
Cite Format: Affinity Biosciences Cat# DF6602, RRID:AB_2838564.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

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;

Immunogens

Immunogen:

A synthesized peptide derived from human COPS5, corresponding to a region within the internal amino acids.

Uniprot:

Q92905(CSN5_HUMAN) >>Visit HPA database.

Gene(ID):
COPS5(10987)
Description:
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).
Sequence:
MAASGSGMAQKTWELANNMQEAQSIDEIYKYDKKQQQEILAAKPWTKDHHYFKYCKISALALLKMVMHARSGGNLEVMGLMLGKVDGETMIIMDSFALPVEGTETRVNAQAAAYEYMAAYIENAKQVGRLENAIGWYHSHPGYGCWLSGIDVSTQMLNQQFQEPFVAVVIDPTRTISAGKVNLGAFRTYPKGYKPPDEGPSEYQTIPLNKIEDFGVHCKQYYALEVSYFKSSLDRKLLELLWNKYWVNTLSSSSLLTNADYTTGQVFDLSEKLEQSEAQLGRGSFMLGLETHDRKSEDKLAKATRDSCKTTIEAIHGLMSQVIKDKLFNQINIS

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Xenopus
100
Zebrafish
100
Chicken
100
Rabbit
100
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

Research Backgrounds

Function:

Probable protease subunit 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 the 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, 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. In the complex, it probably acts as the catalytic center that mediates the cleavage of Nedd8 from cullins. It however has no metalloprotease activity by itself and requires the other subunits of the CSN complex. Interacts directly with a large number of proteins that are regulated by the CSN complex, confirming a key role in the complex. Promotes the proteasomal degradation of BRSK2.

Subcellular Location:

Cytoplasm>Cytosol. Nucleus. Cytoplasm>Perinuclear region. Cytoplasmic vesicle>Secretory vesicle>Synaptic vesicle.
Note: Nuclear localization is diminished in the presence of IFIT3.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Family&Domains:

The JAMM motif is essential for the protease activity of the CSN complex resulting in deneddylation of cullins. It constitutes the catalytic center of the complex (By similarity).

Belongs to the peptidase M67A family. CSN5 subfamily.

References

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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