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Merck
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문서

CSTZFN

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CompoZr® Custom Zinc Finger Nuclease (ZFN)

ZFN plasmid and mRNA

동의어(들):

Zinc Finger Nuclease

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About This Item

UNSPSC 코드:
12352200

제품 라인

CompoZr®

배송 상태

dry ice

저장 온도

−70°C

유사한 제품을 찾으십니까? 방문 제품 비교 안내

일반 설명

Zinc Finger Nucleases (ZFNs) are a class of engineered DNA-binding proteins that facilitate targeted editing of the genome by creating double-strand breaks in DNA at user-specified locations. Double-strand breaks are important for site-specific mutagenesis in that they stimulate the cell′s natural DNA-repair processes, namely homologous recombination and Non-Homologous End Joining (NHEJ). By implementing established, field-proven methods, these processes can be harnessed to generate precisely targeted genomic edits, resulting in cell lines with precise and heritable gene deletions, integrations or modifications.

애플리케이션

Functional Genomics/Target Validation
  • Creation of gene knockouts in multiple cell lines
  • Complete knockout of genes not amenable to RNAi
Cell-based Screening
  • Creation of knock-in cell lines with promoters, fusion tags or reporters integrated into endogenous genes
Cell Line Optimization
  • Creation of cell lines that produce higher yields of proteins or antibodies
The CompoZr Custom ZFN service can be used to target genes from a variety of organisms. Validation of the custom ZFNs is completed in a proxy cell line for human, mouse, rat and hamster (CHO) projects. In this assay, the candidate ZFNs are delivered to the proxy cell line and activity is identified and measured. Activity is measured by amplifying over the ZFN target site and then using a nuclease mismatch enzyme to cut DNA strands that have been modified. ZFN efficiency can be measured based on the densitometry results of this assay. CompoZr Custom ZFN Projects for human, mouse, rat, and hamster (CHO) will have a production timeline of 10 weeks after the ZFN design is approved.

특징 및 장점

  • Rapid design, assembly, and validation of a ZFN pair targeting your gene of interest
  • Rapid and permanent disruption of, or integration into, any genomic loci
  • Mutations made are permanent and heritable
  • Works in a variety of mammalian somatic cell types
  • Edits induced through a single transfection experiment
  • Knockout or knock-in cell lines in as little as two months
  • Single or biallelic edits occur in 1-20% of clone population
  • No antibiotic selection required for screening

성분

  • Best Performing ZFN Pair
  • 10 Aliquots of Ready-to-Deliver ZFN Pair in mRNA form
  • ZFN Pair in Plasmid Form
  • Forward and Reverse Primers that allow for determination of rate of mutation and for screening of individual clones
  • Positive Control DNA
  • Used to determine a baseline cutting efficiency

기타 정보

To have a ZFN made targeting your gene of interest, please inquire about our
Custom ZFN Service offering HERE

법적 정보

All Zinc Finger Nucleases are sold under license from Sangamo Biosciences. For a copy of the Label License provided with purchase of CompoZr ZFNs, please visit the ZFN Label License page.
CompoZr is a registered trademark of Merck KGaA, Darmstadt, Germany

관련 제품

Storage Class Code

10 - Combustible liquids

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.

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문서 라이브러리 방문

Chun Cheng Andy Chen et al.
Physiological genomics, 45(3), 110-118 (2012-12-20)
The present study employed a zinc-finger nuclease strategy to create heterozygous knockout (KO) rats for the transforming growth factor-β1 (Tgfb1) gene on the Dahl SS/Jr genetic background (TGF-β1(+/-) Dahl S). Intercrossing TGF-β1(+/-) rats did not produce any homozygous KO rats
Yoshihiro Inami et al.
The Journal of cell biology, 193(2), 275-284 (2011-04-13)
Suppression of autophagy is always accompanied by marked accumulation of p62, a selective autophagy substrate. Because p62 interacts with the Nrf2-binding site on Keap1, which is a Cullin 3-based ubiquitin ligase adapter protein, autophagy deficiency causes competitive inhibition of the
Bettina Schmid et al.
Proceedings of the National Academy of Sciences of the United States of America, 110(13), 4986-4991 (2013-03-05)
Mutations in the Tar DNA binding protein of 43 kDa (TDP-43; TARDBP) are associated with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with TDP-43(+) inclusions (FTLD-TDP). To determine the physiological function of TDP-43, we knocked out zebrafish Tardbp and
A Tanaka et al.
Leukemia, 27(8), 1621-1627 (2013-02-16)
Human T-cell leukemia virus type 1 (HTLV-1), which causes adult T-cell leukemia (ATL) in humans, establishes a life-long latent infection. Current therapies are not very effective against HTLV-1-associated disorders. A novel therapeutic approach may help to combat HTLV-1 infection. A
David L Mattson et al.
American journal of physiology. Regulatory, integrative and comparative physiology, 304(6), R407-R414 (2013-02-01)
Hypertension and renal damage in Dahl SS rats are associated with increased infiltrating immune cells in the kidney. To examine the role of infiltrating immune cells in this disease process, a zinc finger nuclease targeting bases 672-706 of recombination-activating gene

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