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tebu-bio's SilenciX® stable silenced (knockdown) cellular models

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SilenciX® - a new era in silencing:
for reliable, stable knockdown

What is SilenciX®?

SilenciX® cells are tebu-bio's ready-to-use, knockdown (KD) cell lines using a unique siRNA Delivery system.

The most classic approaches to silencing are based on siRNA but these strategies suffer from lack of stability and efficiency. To overcome this issue, new tools based on short hairpin (shRNA) were developed. These tools increase stability, but disturb genome integrity.

 

Our solution

SilenciX® combines RNAi technology, EBV derived vectors and a Designer of Small Interfering RNA (DSIR) program to generate syngenic, ready-to-use and stable models already validated in the literature and covering various fields of research such as DNA Repair, Epigenetics, Ubiquitination and the cell cycle.

 

Main SilenciX® benefits & advantages

The SilenciX® technology brings stability and efficiency of knockdown in a syngenic model at an affordable cost. 

More than one hundred ready-to-use models with specific and efficient knockdown are already available.

We obtain >80% KD (tebu-bio quality controls are performed by qPCR) leading to very low remaining gene expression in SilenciX®, compared to endogenous expression.

​Stable silencing over time (months) reinforced with hygromycine selection

No integration into the genome - vector remains anchored to the chromosomes giving access to comparable genetic background between cell line control and knock-down.

​Long-term gene silencing without the safety concerns inherent in viral-based siRNA vehicles.

There's a SilenciX® suited to your needs...

       Browse among our 100+ cell lines already available from catalogue
 
        If your target is not available, our product specialists will be more than pleased to suggest
        personalised solutions for your project.

Complete: what you'll receive in your SilenciX® kit...

Ready-to-use: getting started with your SilenciX®...


Flexible: Custom SilenciX® - on simple request

Can't see your SilenciX® in our catalogue? Just let us know your cell type of interest and your target gene and we'll send you a personalised quotation. Our product specialists will be more than pleased to suggest the ideal solutions for your project.

SilenciX® technology has already been shown to be compatible with numerous mammalian cell types including Human, Primate and Rodent cells. 

For further information or for any queries, get in touch with your local tebu-bio's office.

Proven, guaranteed technology:
Main SilenciX® applications

Since they were established, SilenciX® cell lines have been used in a wide variety of fields. They are especially appreciated in genetic disease and cancer studies, where the difficulty is to study protein loss-of-function in a stable genetic background.

A large number of applications directly linked to drug development can be seen in the literature :


Loss-of-function & cell signalling model

Silencing is today the most adopted method to study gene function.

SilenciX® combines RNAi technology, a DSIR Program and a pEBV (Epstein Barr Virus) derived vector to generate functional stable knock-down clones to study protein loss-of-function.

Click here to download our SilenciX® application poster

Nucleocytoplasmic Translocation of UBXN2A Is Required for Apoptosis during DNA Damage Stresses in Colon Cancer Cells.
Abdullah A. et al. (Sept 2015) J. Cancer 2015, 6, 11, 1066–1078. DOI: 10.7150/jca.12134.

UCP2 modulates single-channel properties of a MCU-dependent Ca2+ inward current in mitochondria.
Bondarenko A.I. et al. (2015) Eur. J. Physiol.  467:2509–2518. DOI 10.1007/s00424-015-1727-z.

Poly(ADP-Ribosyl) Glycohydrolase Prevents the Accumulation of Unusual Replication Structures during Unperturbed S Phase.
Chaudhuri A.R. et al. (2015) Mol. Cell. Biol., vol 35, 5, 856-865. DOI: 10.1128/MCB.01077-14.

Supervillin binds the Rac/Rho-GEF Trio and increases Trio-mediated Rac1 activation
Son K. et al.(2015) Cytoskeleton 72, 1, 47–64. DOI: 10.1002/cm.21210.
 
Reversal of mitochondrial defects with CSB-dependent serine protease inhibitors in patient cells of the progeroid Cockayne syndrome
Chatre L. et al. (2015) Proc Natl Acad Sci U.S.A., Jun 2;112(22):E2910-9. DOI: 10.1073/pnas.1422264112. 
 
Glutathione Peroxidase 8 is transcriptionally regulated by HIFa and modulates growth factor signaling in HeLa cells
Bosello-Travaina V. et al. (2015) Free Radical Biology and Medicine, 81, 58-68. DOI:10.1016/j.freeradbiomed.2014.12.020
 
Endonuclease G initiates DNA rearrangements at the MLL breakpoint cluster upon replication stress
Gole B., Baumann C. et al. (2014) Oncogene, pp-1-11. DOI:10.1038/onc.2014.268.
 
Inositol-1,4,5-trisphosphate (IP3)-mediated STIM1 oligomerization requires intact mitochondrial Ca2+ uptake
Deak AT et al. (2014) J Cell Sci. 2014 May 7. DOI: 10.1242/?jcs.149807e.
 
Mitochondrial Ca2+ uniporter (MCU)-dependent and MCU-independent Ca2+ channels coexist in the inner mitochondrial membrane.
Bondarenko AI, et al., European J. Physiol., 2013 Oct. DOI: 10.1007/s00424-013-1383-0

A DNA-dependent stress response involving DNA-PK occurs in hypoxic cells and contributes to cellular adaptation to hypoxia
Bouquet F, et al., J Cell Sci. 2011 Jun 1;124(Pt 11):1943-51

Activation of NRF2 by nitrosative agents and H2O2 involves KEAP1 disulfide formation
Fourquet S. et al., J Biol Chem. 2010 Mar 12;285(11):8463-71

ARTEMIS nuclease facilitates apoptotic chromatin cleavage
Britton S. et al., Cancer Res. 2009 Oct 15;69(20):8120-6

Differential contribution of XPC, RAD23A, RAD23B and CENTRIN 2 to the UV-response in Human cells
Renaud E, et al., DNA Repair 2011 Aug 15;10(8):835-47

Interplay between Cernunnos-XLF and nonhomologous end-joining proteins at DNA ends in the cell
Wu et al., J Biol Chem. 2007 Nov 2;282(44):31937-43

Long-term XPC silencing reduces DNA double-strand break repair
Despras et al., Cancer Res. 2007; 67: 2526-2534.

Loss of ATM positively regulates the expression of Hypoxia Inducible Factor 1 (HIF-1) through oxidative stress: role in the physiopathology of the disease
Ousset M, et al., Cell Cycle 2010 Jul 3;9 (14)

NER factors are recruited to active promoters and facilitate chromatin modification for transcription in the absence of exogenous genotoxic attack
Le May N. et al., Mol Cell. 2010 Apr 9;38(1):54-66

Partial complementation of a DNA ligase I deficiency by DNA ligase III and its impact on cell survival and telomere stability in mammalian cells
Le Chalony, et al., Cell Mol Life Sci. 2012

Poly (ADP-Ribose) Glycohydrolase Regulates Retinoic Acid Receptor-Mediated Gene Expression
Le May N, Mol Cell. 2012 Oct 24. pii: S1097-2765(12)00821-0. doi:
10.1016/j.molcel.2012.09.021

Role of ATM in the telomere response to the G-quadruplex ligand 360A
Pennarun G. et al., Nucleic Acids Res. 2008 Mar;36(5):1741-54

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Synthetic Lethality

Synthetic lethality occurs when 2 separate genes compensate for each other in term of function:

One of the challenges in this approach is to validate synthetic lethal genes.

Our solution has been to design SilenciX® cell lines in which a gene known to be implicated in synthetic lethality is already silenced.

By comparing the control and the silenced cell lines, the target can be easily explored.

Examples of SilenciX® for Synthetic Lethality studies

Target Name Level of KD Cat. Nr.
BRCA1 86% 01-00041
BRCA2 72% 01-00028
XRCC1 87% 01-00017
PARP1 97% 01-00019
PARP2 86% 01-00020
APE1 >70% 01-00155

 

 

 

 

 

 

 

        tebu-bio quality controls are performed by qPCR

New publication using the SilenciX cellular models:

Cellularly active N-hydroxyurea FEN1 inhibitors block substrate entry to the active site.
Exell J.C. et al. (August 2016) Nature Chemical Biology 12, 815–821 (2016) doi:10.1038/nchembio.2148.

SilenciX®, novel stable knock-down cellular models to screen new molecular targets through the synthetic lethality approach  (AACR 2014, San Diego) Abstract n° 3733
Eric Mennesson1, Anne-Marie Renault1, Isabelle Fixe1, Catherine Grillon2, Claudine Kiéda2, Nadia Normand1
1/ tebu-bio (France) 2/ Centre de Biophysique Moléculaire, CNRS UPR 4301 (France)

A BRCA2 specific knoch-down stable cellular model to screen molecular targets with the Synthetic Lethality approach. Anne Marie Renault (tebu-bio), Helen Robinson (MISSION Therapeutics), et al. (poster at the  Cancer Pharmacogenomics and Targeted Therapies congress).  September 2013

Inhibition of DNA damage repair by artificial activation of PARP with siDNA.
Croset A, et al. Nucleic Acids Res. 2013 August.

Synthetic lethal targeting of DNA double-strand break repair deficient cells by human apurinic/apyrimidinic endonuclease inhibitors.
Sultana, et al. Int J Cancer. 2012 Nov 15;131(10):2433-44. doi:10.1002/ijc.27512. Epub 2012 Mar 28.

Targeting XRCC1 deficiency in breast cancer for personalized therapy.
Sultana R, et al. Cancer Res. 2012 Dec 19.

Clinicopathological and functional significance of XRCC1 expression in ovarian cancer.
Abdel-Fatah T, et al.Int J Cancer. 2012 Dec 6. doi: 10.1002/ijc.27980.
 
Back to Main SilenciX®Applications  -  Back to top of page
 

Personalized medicine

New tools in molecular biology have given rise to of a new area of research: personalized medicine.

It is a customization of healthcare with decision and practices being tailored to the individual patient by use of genetic or other information (Biomarkers). Combining this information gives an indication of whether there is a threat for disease, whether a disease already exists, or how such disease may develop in an individual case.

The discovery of polymorphism in genes that function in the metabolism of chemicals and in DNA repair has demonstrated the importance of understanding the phenomenon of genetic susceptibility in a population.

Another incoming important challenge in personalized medicine and in drug discovery is the prediction of the population on which a drug can be used. The sooner this evaluation is done in development, the more adapted the process can be.

A new application of SilenciX® is to allow researchers to test their components on a cell line which mimics the population of interest.

Examples of SilenciX® for Personalised Medicine studies

Target Name Level of KD Cat. Nr.
BRCA1 86% 01-00041
BRCA2 72% 01-00028
XRCC1 87% 01-00017
OGG1 97% 01-00014
NEIL2 81% 01-00053
MSH2 91% 01-00023
MLH1 >70% 01-00147

 

 

 

 

 

 

 

 

        tebu-bio quality controls are performed by qPCR

Targeting BRCA1-BER deficient breast cancer by ATM or DNA-PKcs blockade either alone or in combination with cisplatin for personalized therapy.
Albarakatia N. et al. (2015) Molecular Oncology 9, 1, 204–217. DOI:10.1016/j.molonc.2014.08.001.

​Long-term XPC silencing reduces DNA double-strand break repair.
Despras et al., Cancer Res. 2007; 67: 2526-2534.

Oxidation-mediated DNA cross-linking contributes to the toxicity of 6-thioguanine in human cells.
Brem, et al. Cancer Res. 2012 Sep

Synthetic lethal targeting of DNA double-strand break repair deficient cells by human purinic/apyrimidinic endonuclease inhibitors.
Sultana, et al. Int J Cancer. 2012 Nov 15;131(10):2433-44. doi:10.1002/ijc.27512. Epub 2012 Mar 28.

The impact of cyclin-dependent kinase 5 depletion on poly(ADPribose) polymerase activity and responses to radiation.
Bolin C, et al., Cell Mol Life Sci. 2011 Sept 16.

Clinicopathological and functional significance of XRCC1 expression in ovarian cancer.
Abdel-Fatah T, et al. Int J Cancer. 2012 Dec 6. doi: 10.1002/ijc.27980.

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Drug Selectivity

To allow researchers to verify the efficiency of inhibitors, we have developed a family of cell lines for new attractive targets in research.

Examples of SilenciX® for Drug Selectivity studies

Target Name Level of KD Cat. Nr.
USP7 74% 01-00159
USP9X 73% 01-00160
DNA-PKcs 93% 01-00005
APE1 >70% 01-00155
PARP1 97% 01-00019
PARP2 86% 01-00020

 

 

 

 

 

 

 

        tebu-bio quality controls are performed by qPCR

Back to Main SilenciX®Applications  -  Back to top of page


Human disease mimicking model

Comparison of cells derived from patients with the same phenotype or disease can be problematic due to their different genetic backgrounds.

SilenciX® cell lines mimic the behavior of cells derived from patients and enable you to assess the long-term consequences of gene silencing in a robust model.

Click here to download our SilenciX® application poster

Examples of SilenciX® for Human Disease Mimicking Models

Target Name Level of KD Cat. Nr.
XPA 78% 01-00015
XPC 81% 01-00016
ATR 70% 01-00025
ATM 88% 01-00029
BRCA1 86% 01-00041
BRCA2 72% 01-00028
FANCD1 85% 01-00027

 

 

 

 

 

 

 

 

        tebu-bio quality controls are performed by qPCR

ATR contributes to telomere maintenance in human cells
Pennarun G. et al., Nucleic Acids Res. 2010 May;38(9):2955-63

Long-term XPC silencing reduces DNA double-strand break repair.
Despras et al., Cancer Res. 2007; 67: 2526-2534.

Loss of ATM positively regulates the expression of Hypoxia Inducible Factor 1 (HIF-1) through oxidative stress: role in the physiopathology of the disease
Ousset M, et al., Cell Cycle 2010 Jul 3;9 (14)

NER factors are recruited to active promoters and facilitate chromatin modification for transcription in the absence of exogenous genotoxic attack
Le May N. et al., Mol Cell. 2010 Apr 9;38(1):54-66

NF-κB regulates DNA double-strand break repair in conjunction with BRCA1–CtIP complexes
Volcic, et al. Nucleic Acids Res. (2012)

Untangling the relationships between DNA repair pathways by silencing more than 20 DNA repair genes in human stable clones.
Biard, Nucleic Acids Res. 2007;35(11):3535-50

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Therapy Combination

SilenciX® has been used to find genes that, when silenced, result in sensitivity to certain chemotherapy treatments. Researchers therefore can further characterize drug-sensitive targets and novel drug combinations that sensitize cancer cells to chemotherapeutic drugs.

More than 100 cell lines are already available from catalogue, or get in touch with our specialists for your custom requests.

PRX1 knockdown potentiates vitamin K3 toxicity in cancer cells: a potential new therapeutic perspective for an old drug.
Tiantian, H. at al. Journal of Experimental & Clinical Cancer Research (2015) 34:152 DOI: 10.1186/s13046-015-0270-2.

The impact of cyclin-dependent kinase 5 depletion on poly(ADPribose) polymerase activity and responses to radiation.
Bolin C, et al., Cell Mol Life Sci. 2011 Sept 16.

Back to Main SilenciX®Applications  -  Back to top of page


SilenciX® is a registered trademark of tebu-bio; technology licensed from the Atomic Energy and Alternative Energies Commission (CEA). CEA logo

 

To order your SilenciX®

tebu-bio - innovative reagents and lab services including stable silenced cell lines SilenciX

tebu-bio - Anne-Marie Renault (Business Development SilenciX®)

 

United States of America and Canada:

LifeSensors SilenciX tebu-bio

LifeSensors - info @ lifesensors.com

Japan:

Funakoshi - jutaku @ funakoshi.co.jp Funakoshi SilenciX tebu-bio


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