Upstream / Downstream

Explore pathways related to this product.

Antibody Guarantee

CST Antibody Performance Guarantee

LEARN MORE  

To Purchase # 8345S

8345S 1 Kit (4 x 40 µl) $329.00
$ 0. 00

Questions?

Find answers on our FAQs page.

ANSWERS  

Visit PhosphoSitePlus®

PTM information and tools available.

LEARN MORE

Product Includes Quantity Applications Reactivity MW(kDa) Isotype
COPS5 Antibody 6895 40 µl
H M R Mk 37 Rabbit 
p27 Kip1 (D69C12) XP® Rabbit mAb 3686 40 µl
H R Mk 27 Rabbit IgG
Smad4 Antibody 9515 40 µl
H M R Mk 70 Rabbit 
p53 (7F5) Rabbit mAb 2527 40 µl
H Mk 53 Rabbit IgG
Anti-rabbit IgG, HRP-linked Antibody 7074 100 µl
All Goat 

Product Description

The Tumor Suppressor Inactivation Antibody Sampler Kit provides a fast and economical means of evaluating the role of COPS5 in the inhibition of the tumor suppressors p27 Kip1, p53, and Smad4. The kit contains enough primary antibody to perform four western blot experiments with each primary antibody.


Specificity / Sensitivity

COPS5 Antibody recognizes endogenous levels of total COPS5 protein. This antibody does not cross-react with PSMD14/POH1. p27 Kip1 (D69C12) XP® Rabbit mAb detects endogenous levels of total p27 Kip1 protein. p53 (7F5) Rabbit mAb detects endogenous levels of total p53 protein. This antibody binding has been mapped to the amino terminal region of human p53 protein. Smad4 Antibody detects endogenous levels of total Smad4 protein.


Source / Purification

Monoclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human p27 Kip1 protein or with a full-length human p53 fusion protein. Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human COPS5 protein or to the residues surrounding Pro278 of human Smad4 protein. Polyclonal antibodies are purified by protein A and peptide affinity chromatography.

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 (1). 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 (2). Indeed, COPS5 harbors an Mpr1-Pad1-N-terminal (MPN) domain with an embedded Jab1/CSN5 MPN domain metalloenzyme (JAMM) motif that is essential for the CSN isopeptidase activity responsible for deneddylation of CRLs. COPS5 is an evolutionarily conserved 38 kDa protein in humans, mice, fission yeast, and plants, which suggests that it is critical to cell survival and proliferation. A role for COPS5 as a positive regulator of cellular proliferation is supported by evidence that it functionally inactivates several key tumor suppressors such as p53, RUNX3, Smad4, and p27 Kip1 through altered subcellular localization, degradation, and deneddylation (3-7). These findings are underscored by the observation that COPS5 overexpression has been identified in a number of different tumor types and has been implicated in the initiation and progression of several types of cancer (8). Moreover, COPS5 deficient mice display an embryonically lethal phenotype highlighted by elevated expression of COPS5 targets such as p53 and p27 (9,10).


1.  Claret, F.X. et al. (1996) Nature 383, 453-7.

2.  Wei, N. et al. (2008) Trends Biochem Sci 33, 592-600.

3.  Bech-Otschir, D. et al. (2001) EMBO J 20, 1630-9.

4.  Oh, W. et al. (2006) J Biol Chem 281, 17457-65.

5.  Wan, M. et al. (2002) EMBO Rep 3, 171-6.

6.  Tomoda, K. et al. (2002) J Biol Chem 277, 2302-10.

7.  Kim, J.H. et al. (2009) J Cell Biochem 107, 557-65.

8.  Shackleford, T.J. and Claret, F.X. (2010) Cell Div 5, 26.

9.  Tian, L. et al. (2010) Oncogene 29, 6125-37.

10.  Tomoda, K. et al. (2004) J Biol Chem 279, 43013-8.


Entrez-Gene Id 10987, 1027, 7157, 4089
Swiss-Prot Acc. Q92905, P46527, P04637, Q13485

Protein Specific References

Chehab NH et al. (1999) Proc Natl Acad Sci U S A 96, 13777–82

Buschmann T et al. (2000) Cancer Res 60, 896–900

Chehab NH et al. (2000) Genes Dev 14, 278–88

Persons DL et al. (2000) J Biol Chem 275, 35778–85

Vaziri H et al. (2001) Cell 107, 149–59

Minamoto T et al. (2001) Oncogene 20, 3341–7

Stewart ZA et al. (2001) Oncogene 20, 113–24

Bean LJ and Stark GR (2001) Oncogene 20, 1076–84

Xie S et al. (2001) J Biol Chem 276, 43305–12

Xie S et al. (2001) J Biol Chem 276, 36194–9

Kim SJ et al. (2002) J Biol Chem 277, 33501–8

Bulavin DV et al. (2002) Nat Genet 31, 210–5

Shono T et al. (2002) Cancer Res 62, 1069–76

Adamson AW et al. (2002) J Biol Chem 277, 38222–9

Hase H et al. (2002) J Biol Chem 277, 46950–8

Bischof O et al. (2002) EMBO J 21, 3358–69

Qin JZ et al. (2002) Oncogene 21, 2991–3002

Hofmann TG et al. (2002) Nat Cell Biol 4, 1–10

Chouinard N et al. (2002) Biochem J 365, 133–45

Shiseki M et al. (2003) Cancer Res 63, 2373–8

Chen K et al. (2003) J Biol Chem 278, 39527–33

Sengupta S et al. (2003) EMBO J 22, 1210–22

Urban G et al. (2003) J Biol Chem 278, 9747–53

Oguchi K et al. (2003) Blood 101, 3622–7

Hideshima T et al. (2003) Blood 101, 1530–4

Lindström MS and Wiman KG (2003) Oncogene 22, 4993–5005

Hofseth LJ et al. (2003) Proc Natl Acad Sci U S A 100, 143–8

Wang C and Chen J (2003) J Biol Chem 278, 2066–71

Matsuoka M et al. (2003) Environ Health Perspect 111, 509–12

Yanamadala S and Ljungman M (2003) Mol Cancer Res 1, 747–54

Möller A et al. (2003) Cancer Res 63, 4310–4

Goudelock DM et al. (2003) J Biol Chem 278, 29940–7

Louria-Hayon I et al. (2003) J Biol Chem 278, 33134–41

Tritarelli A et al. (2004) Mol Biol Cell 15, 3751–7

Mroz RM et al. (2004) Am J Respir Cell Mol Biol 30, 564–8

Rui Y et al. (2004) EMBO J 23, 4583–94

Li Y et al. (2004) Oncogene 23, 7355–65

Vaghefi H and Neet KE (2004) Oncogene 23, 8078–87

Nair VD et al. (2004) J Biol Chem 279, 27494–501

Takagi M et al. (2004) Blood 103, 283–90

Ito K et al. (2004) Cancer Res 64, 1071–8

Koutsodontis G and Kardassis D (2004) Oncogene 23, 9190–200

Jackson MW et al. (2004) Oncogene 23, 4477–87

Dohoney KM et al. (2004) Oncogene 23, 49–57

Thompson T et al. (2004) J Biol Chem 279, 53015–22

Yeh PY et al. (2004) Oncogene 23, 3580–8

Komiyama S et al. (2004) Biochem Biophys Res Commun 323, 816–22

Soubeyrand S et al. (2004) Eur J Biochem 271, 3776–84

Ou YH et al. (2005) Mol Biol Cell 16, 1684–95

Feki A et al. (2005) Oncogene 24, 3726–36

Li Z et al. (2005) J Biol Chem 280, 16843–50

Di Stefano V et al. (2005) Oncogene 24, 5431–42

Hershko T et al. (2005) Cell Death Differ 12, 377–83

Mayo LD et al. (2005) J Biol Chem 280, 25953–9

Wesierska-Gadek J et al. (2005) Mol Cancer Ther 4, 113–24

Wang L et al. (2005) Oncogene 24, 3020–7

Zhao Y et al. (2006) Mol Cell Biol 26, 2782–90

Gresko E et al. (2006) EMBO J 25, 1883–94

Ichwan SJ et al. (2006) Oncogene 25, 1216–24

Knights CD et al. (2006) J Cell Biol 173, 533–44

Moiseeva O et al. (2006) Mol Biol Cell 17, 1583–92

Zeng PY and Berger SL (2006) Cancer Res 66, 10701–8

Li AG et al. (2006) Mol Cell 23, 575–87

Yoshida K et al. (2006) J Biol Chem 281, 5734–40

Li DW et al. (2006) Oncogene 25, 3006–22

Fraser M et al. (2006) Oncogene 25, 2203–12

Paulsen MT et al. (2006) Mol Cancer 5, 25

Singh K et al. (2007) PLoS One 2, e660

Nag A et al. (2007) J Biol Chem 282, 8812–20

Li HH et al. (2007) EMBO J 26, 402–11

Li Q et al. (2007) Cancer Res 67, 66–74

Taira N et al. (2007) Mol Cell 25, 725–38

Lambrot R et al. (2007) J Clin Endocrinol Metab 92, 2632–9

Ivanov GS et al. (2007) Mol Cell Biol 27, 6756–69

Nakanishi M et al. (2007) J Biol Chem 282, 22993–3004

Liu Y et al. (2007) J Biol Chem 282, 2505–11

Derheimer FA et al. (2007) Proc Natl Acad Sci U S A 104, 12778–83

Lee JH et al. (2007) J Cell Sci 120, 2259–71

Mantovani F et al. (2007) Nat Struct Mol Biol 14, 912–20

Wang H et al. (2008) J Biol Chem 283, 2564–74

Sun L et al. (2008) J Exp Clin Cancer Res 27, 35

Chang PC and Li M (2008) J Virol 82, 278–90

Lin T et al. (2008) Toxicology 247, 145–53

Chen JJ et al. (2008) J Immunol 180, 8030–9

Shouse GP et al. (2008) Mol Cell Biol 28, 448–56

Kitagawa M et al. (2008) Mol Cell 29, 217–31

Habold C et al. (2008) J Cell Mol Med 12, 607–21

Zhu H et al. (2008) Int J Cancer 123, 2741–9

Yamaguchi H et al. (2009) J Biol Chem 284, 11171–83

Wang Z et al. (2009) Pharm Res 26, 1140–8

Bar JK et al. (2009) Int J Gynecol Cancer 19, 1322–8

Nishimura T et al. (2009) J Biol Chem 284, 36442–52

Puca R et al. (2009) Mol Cancer 8, 85

Yadavilli S et al. (2009) J Biochem Mol Toxicol 23, 373–86

Baxter EW and Milner J (2010) J Neurooncol 97, 373–82

Fraser JA et al. (2010) J Biol Chem 285, 37773–86

Fraser JA et al. (2010) J Biol Chem 285, 37762–72

Shang X et al. (2010) Oncogene 29, 4938–46

Chen X et al. (2010) J Biol Chem 285, 12823–30

Kawano T et al. (2010) Int J Oncol 37, 787–95

Moehlenbrink J et al. (2010) Cancer Lett 292, 119–24

Venerando A et al. (2010) Cell Mol Life Sci 67, 1105–18

Puca R et al. (2010) Free Radic Biol Med 48, 1338–46

Marchenko ND et al. (2010) Cell Death Differ 17, 255–67

Aranha MM et al. (2011) PLoS One 6, e21396

Muñoz-Fontela C et al. (2011) Cell Cycle 10, 3701–5

Wu L et al. (2011) J Biol Chem 286, 2236–44

Ozeki C et al. (2011) J Biol Chem 286, 18251–60

Mellert HS et al. (2011) J Biol Chem 286, 4264–70

Valbuena A et al. (2011) PLoS One 6, e17320

Xu S et al. (2011) J Cardiovasc Pharmacol 58, 263–71

Seo SK et al. (2011) J Thorac Oncol 6, 1313–9

Savelyeva I and Dobbelstein M (2011) Oncogene 30, 865–75

Wu ZZ et al. (2011) J Cell Physiol 226, 2415–28

Smeenk L et al. (2011) PLoS One 6, e17574

Grison A et al. (2011) Proc Natl Acad Sci U S A 108, 17979–84

Gully CP et al. (2012) Proc Natl Acad Sci U S A 109, E1513–22

Wang H et al. (2012) DNA Repair (Amst) 11, 146–56

Xu S et al. (2013) Cell Res 23, 423–35

Chan C et al. (2013) Mol Cell Biol 33, 485–97

Thakur BK et al. (2013) Int J Cancer 132, 766–74

Yang Y et al. (2013) J Biol Chem 288, 529–39

Ohshima T and Shimotohno K (2003) J Biol Chem 278, 50833–42


For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.
U.S. Patent No. 5,675,063.