FZR1基因敲除质粒

pLenti-FZR1-sgRNA (FZR1基因敲除质粒)是一种在动物细胞中可以同时表达Cas9、目的基因的sgRNA和puromycin抗性基因的质粒。用于在动物细胞中直接基于CRISPR/Cas9技术敲除目的基因，或者通过包装慢病毒后基于CRISPR/Cas9技术敲除目的基因。本质粒中sgRNA的有效性已经通过T7EI法的验证。

本质粒在细菌中为Amp抗性，全长约13,000bp。本质粒的关键图谱信息请参考图1。本质粒可直接转染细胞用于目的基因的CRISPR/Cas9敲除，以及通过puromycin筛选稳定细胞株；也可以与pMDLg、Rev及VSV-g共转HEK293T细胞进行重组慢病毒(lentivirus)的包装，然后再用于感染细胞或组织并进行目的基因的CRISPR/Cas9敲除。

图1. 表达sgRNA、Cas9和puromycin抗性的pLenti-sgRNA质粒关键图谱信息。

本质粒中的sgRNA基于碧云天研发的CRISPR/Cas9 sgRNA快速筛选和验证体系获得，sgRNA的有效性已经通过T7EI法验证。

本质粒用于实验时，建议同时选购无任何靶向的对照质粒pLenti-Control-sgRNA (L00011)或靶向GFP的对照质粒pLenti-GFP-sgRNA (L00013)。

碧云天同时提供基于CRISPR/Cas9技术的FZR1基因敲除的质粒(L22100 pLenti-FZR1-sgRNA)、慢病毒(L22101 FZR1 Knockout Lentivirus)、HEK293T细胞(L22102 FZR1 Knockout HEK293T Cells)、HEK293T敲除细胞的RIPA裂解液(L22103 FZR1 Knockout HEK293T RIPA Lysate)、HEK293T敲除细胞的Trizol裂解液(L22104 FZR1 Knockout HEK293T Trizol Lysate)等产品，具体请在碧云天网站查询或在本产品网页点击相应产品。

FZR1基因的基本信息如下：

Species	Gene Symbol	Gene ID	GenBank Accession	Transcript
Human	FZR1	51343	BC013413	NM_016263

 

About the gene
Official Symbol	FZR1
Previous Symbol	-
Official Full Name	fizzy and cell division cycle 20 related 1
Synonyms	HCDH1; CDH1; HCDH; FZR; FZR2; KIAA1242; CDC20C
Location	19p13.3
Gene Type	protein-coding gene
Uniprot ID	Q9UM11
Pathway/Library	Cell Cycle Pathway Genes Library
Gene Summary	Substrate-specific adapter for the anaphase promoting complex/cyclosome (APC/C) E3 ubiquitin-protein ligase complex. Associates with the APC/C in late mitosis, in replacement of CDC20, and activates the APC/C during anaphase and telophase. The APC/C remains active in degrading substrates to ensure that positive regulators of the cell cycle do not accumulate prematurely. At the G1/S transition FZR1 is phosphorylated, leading to its dissociation from the APC/C. Following DNA damage, it is required for the G2 DNA damage checkpoint: its dephosphorylation and reassociation with the APC/C leads to the ubiquitination of PLK1, preventing entry into mitosis. Acts as an adapter for APC/C to target the DNA-end resection factor RBBP8/CtIP for ubiquitination and subsequent proteasomal degradation. Through the regulation of RBBP8/CtIP protein turnover, may play a role in DNA damage response, favoring DNA double-strand repair through error-prone non-homologous end joining (NHEJ) over error-free, RBBP8-mediated homologous recombination (HR) (PubMed:25349192). FZR1_HUMAN,Q9UM11