단일뉴클레오티드다형성(SNPs, single-nucleotide polymorphisms)은 집단 다양성과 질병 임상 발현의 주요 요인으로 개별화 의료에서 중요한 역할을 하는 것으로 알려져 있습니다.연구자들은 코호트(cohort)로부터 임상 샘플을 받아 2세대 시퀀스와 전유전체연관(GWA, Genome-Wide Association) 분석을 통해 대량의 SNP 후보 위치(locus)를 생성할 수 있습니다.그러나 SNP 위치와 임상증상 사이의 관계는 체내에서 연구해야 한다. 마우스에서 이러한 SNP 가 발견되면 점 돌연변이 마우스 모델은 임상 연구에 중요한 정보를 제공할 수 있습니다.

Cyagen 이 자체 개발한 점 돌연변이 마우스 모델 데이터베이스를 사용하여 당신의 SNP 연구를 추진합니다. 이 데이터베이스는 인간 SNP 후보점에 해당하는 마우스 돌연변이 지점을 신속하게 식별하고 돌연변이 마우스 모델 전략을 생성합니다.추가적인 임상연구, 정확한 의학, 신약연구를 위해 15% off에 달하는 점 돌연변이 마우스를 제공합니다!

주문 문의는 86 20-31601779로 전화하거나 service-apac@cyagen.com으로 메일 보내주시기 바랍니다.

■ 프로모션 시간: 2022년 5월 16일 - 2022년 7월 31일

■ 프로모션 대상: 한국 지역의 단말 고객, 기타 지역은 저희에게 연락 주십시오.

Service Name	Number of Projects	Promotion Price (USD/Strain)	Promotional Savings
CRISPR-Pro Point Mutation Mice	1-2 Projects	$13,000	Save up to $3000
CRISPR-Pro Point Mutation Mice	≥3 Projects	$12,000	Save up to $10000
CRISPR-Pro Point Mutation Mice	≥5 Projects	$11,250	Save over $16000+

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Cyagen Knockout Catalog Models

10,000+ KO Mouse Strains (Cryopreserved Sperms) | 5,000+ cKO Mouse Strains (Cryopreserved Sperms) | 2000+ KO Live Mouse Strains

Case Study

Cyagen offers rapid point mutation mouse model generation via CRISPR/Cas9-mediated genome editing technology by co-injecting nuclease and oligo donors carrying the desired mutation and homology arms. In this case, the Calca gene was chosen as a target, and guide RNAs (gRNAs) were designed. The gRNA, the donor oligo containing mutation and synonymous mutation (c.1138_1139 [TG to CC]), and Cas9 were co-injected into fertilized mouse eggs to generate targeted point mutation knockin offspring.

Diagram 1. The schematic describes the first stage in developing a point mutation mouse model via CRISPR.

PCR Results:

Figure 1. PCR genotype screening of the F1 mice. Agarose gel electrophoresis of PCR results in F1 mice (#2, 4, 5, 8, and others) with site-specific gene knock-in.

The PCR product will be used for sequencing confirmation.

Figure 2. Representative illustration sequence analyses of F1 mice confirm F1 animals 2, 4, 5, and 8 with c.1138_1139 (TG to CC) mutation.

Publications

Peng, Kun et al. “MAdCAM-1 mediates retinal neuron degeneration in experimental colitis through recruiting gut-homing CD4+ T cells.” Mucosal immunology vol. 14,1 (2021): 152-163. doi:10.1038/s41385-020-0282-x
Di Genua, Cristina et al. “C/EBPα and GATA-2 Mutations Induce Bilineage Acute Erythroid Leukemia through Transformation of a Neomorphic Neutrophil-Erythroid Progenitor.” Cancer cell vol. 37,5 (2020): 690-704.e8. doi:10.1016/j.ccell.2020.03.022
de Bellis, Manuela et al. “Orthogonal arrays of particle assembly are essential for normal aquaporin-4 expression level in the brain.” Glia vol. 69,2 (2021): 473-488. doi:10.1002/glia.23909
Rasmussen, Marit et al. “PARP7 and Mono-ADP-Ribosylation Negatively Regulate Estrogen Receptor α Signaling in Human Breast Cancer Cells.” Cells vol. 10,3 623. 11 Mar. 2021, doi:10.3390/cells10030623
Škorić-Milosavljević, Doris et al. “Rare variants in KDR, encoding VEGF Receptor 2, are associated with tetralogy of Fallot.” Genetics in medicine : official journal of the American College of Medical Genetics vol. 23,10 (2021): 1952-1960. doi:10.1038/s41436-021-01212-y
Liu, Jun et al. “OSMRβ mutants enhance basal keratinocyte differentiation via inactivation of the STAT5/KLF7 axis in PLCA patients.” Protein & cell vol. 12,8 (2021): 653-661. doi:10.1007/s13238-020-00818-3
Wang, Wencai et al. “Mutation-induced DNMT1 cleavage drives neurodegenerative disease.” Science advances vol. 7,36 (2021): eabe8511. doi:10.1126/sciadv.abe8511
Sun, Gan et al. “Loss of Function Mutation in ELF4 Causes Autoinflammatory and Immunodeficiency Disease in Human.” Journal of clinical immunology, 10.1007/s10875-022-01243-3. 9 Mar. 2022, doi:10.1007/s10875-022-01243-3
Bieri, Cornelia et al. “The human pathogenic 91del7 mutation in SLC34A1 has no effect in mineral homeostasis in mice.” Scientific reports vol. 12,1 6102. 12 Apr. 2022, doi:10.1038/s41598-022-10046-w
Dai, Lei et al. “A Biallelic Frameshift Mutation in Nephronectin Causes Bilateral Renal Agenesis in Humans.” Journal of the American Society of Nephrology : JASN vol. 32,8 (2021): 1871-1879. doi:10.1681/ASN.2020121762

FAQ

Where do your mice come from?

Our main source of mice is Charles River Laboratory. Currently, only mice from Charles River laboratory, Jackson Laboratory and Taconic are allowed into our facility.

How do you generate conditional point mutant mice?

Conditional point mutant mice can be generated by introducing the Cre-Loxp system. A conditional point mutation mouse model introduces a point mutation only when certain conditions are met. When Cre recombinase is present, a point mutation will be introduced into the mouse genome tissue specifically via Cre activity. This is done by introducing the targeting vector containing the point mutation, along with strategic use of the Lox regions (known as ‘floxing’ genes). When desired, Cre expression can be induced, which will ultimately lead to activation of transcription of the gene containing the point mutation.

How do you identify point mutant knock-in mice generated using CRISPR?

Since the point mutation is only the addition, deletion, or substitution of a single base or a few bases, the size of the mutant fragment and the wild-type band are indistinguishable on the electropherogram. Therefore, it cannot be identified by PCR alone, and it needs to be confirmed with sequencing to identify the point mutation was successful.

Promotion for Conditional Knockout Mice

조건 녹아웃 마우스는 많은 연구 분야의 생물의학 진전에서 중요한 역할을 하는데, 이는 인간의 질병을 이해하고 약물 개발을 가속화하는 데 매우 중요합니다. cKO/floxed 모델은 전통적인 녹아웃 마우스에 비해 유전자 발현에 대한 정확한 시간과 공간 제어로 실험력이 더 뛰어났습니다.

제한된 시간 내에 10,000달러있으면, Cyagen AI 녹아웃 마우스 모델 eBank당신의 조건 녹아웃 마우스를 얻을 수 있습니다.이번 기회를 놓치지 마세요.

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