PABPC4基因敲除HEK293细胞
货号:
EDJ-KQ6352
物种:
人
细胞名称:
HEK293
基因名称:
PABPC4
基因ID:
8761
规格:
1×10⁶cells
PABPC4基因敲除细胞HEK293是由艾迪基因优化的CRISPR/Cas9编辑而成，采用Sanger测序法验证敲除，保证单克隆，活性良好。
| 货号 | EDJ-KQ6352 |
|---|---|
| 产品名称 | PABPC4 Knockout HEK293 Cell Line |
| 细胞 | HEK293 |
| Cellosaurus ID | CVCL_0045 |
| 细胞别名 | Hek293, HEK-293, HEK/293, (HEK)293, HEK 293, HEK,293, 293, 293 HEK, 293 Ad5, Graham 293, Graham-293, Human Embryonic Kidney 293 |
| 基因 | PABPC4 |
| 基因ID | |
| 基因别名 | APP-1|APP1|PABP4|iPABP |
| 摘要 |
Poly(A)-binding proteins (PABPs) bind to the poly(A) tail present at the 3-prime ends of most eukaryotic mRNAs. PABPC4 or IPABP (inducible PABP) was isolated as an activation-induced T-cell mRNA encoding a protein. Activation of T cells increased PABPC4 mRNA levels in T cells approximately 5-fold. PABPC4 contains 4 RNA-binding domains and proline-rich C terminus. PABPC4 is localized primarily to the cytoplasm. It is suggested that PABPC4 might be necessary for regulation of stability of labile mRNA species in activated T cells. PABPC4 was also identified as an antigen, APP1 (activated-platelet protein-1), expressed on thrombin-activated rabbit platelets. PABPC4 may also be involved in the regulation of protein translation in platelets and megakaryocytes or may participate in the binding or stabilization of polyadenylates in platelet dense granules. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. This protein has also been found to interact with coronavirus nucleocapsid proteins and is thought to inhibit coronavirus replication. [provided by RefSeq, Nov 2021]
|
| 癌症类型 | Non-tumor |
| 细胞形态 | Adherent |
| 传代比率 | 1/2~1/4 |
| 完全培养基 | DMEM + 10% FBS |
| 冻存培养基 | 95%完全培养基+ 5% DMSO |
* 仅供科研使用，不适用于人体或动物，包括临床、治疗或诊断用途。
| Loci | 送检细胞STR信息 送检细胞名: HEK293 | 细胞库细胞STR信息 细胞库细胞名: HEK293 | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | X | ||
| CSF1P0 | 12 | 11 | 12 | |
| D2S1338 | 19 | 19 | ||
| D3S1358 | 15 | 17 | 15 | 17 |
| D5S818 | 8 | 8 | 9 | |
| D7S820 | 11 | 12 | 11 | 12 |
| D8S1179 | 12 | 14 | 12 | 14 |
| D13S317 | 12 | 14 | 12 | 14 |
| D16S539 | 9 | 13 | 9 | 13 |
| D18S51 | 17 | 18 | 17 | 18 |
| D19S433 | 15 | 18 | 15 | 18 |
| D21S11 | 28 | 30.2 | 28 | 30.2 |
| FGA | 23 | 23 | ||
| Penta D | 9 | 10 | 9 | 10 |
| Penta E | 7 | 15 | 7 | 15 |
| TH01 | 7 | 9.3 | 7 | 9.3 |
| TPOX | 11 | 11 | ||
| vWA | 16 | 19 | 16 | 19 |
| D6S1043 | 11 | 11 | ||
| D12S391 | 19 | 21 | 11 | 15 |
| D2S441 | 11 | 15 | 11 | 15 |
* 该细胞系与收录于ATCC, DSMZ, JCRB 和 RIKEN数据库的细胞系STR数据匹配。
结论：该细胞 STR 鉴定正确。
结论：该细胞 STR 鉴定正确。
* 研究用途免责声明：本内容基于公开的研究数据、生物信息学资源及计算分析生成，仅供研究参考。
相关研究文献
MKRN3 介导的 Poly (A) 结合蛋白泛素化调节哺乳动物青春期 GNRH1 mRNA 的稳定性和翻译。
IF=13.1
Nucleic acids research
The family of Poly(A)-binding proteins (PABPs) regulates the stability and translation of messenger RNAs (mRNAs). Here we reported that the three members of PABPs, including PABPC1, PABPC3 and PABPC4, were identified as novel substrates for MKRN3, whose deletion or loss-of-function mutations were genetically associated with human central precocious puberty (CPP). MKRN3-mediated ubiquitination was found to attenuate the binding of PABPs to the poly(A) tails of mRNA, which led to shortened poly(A) tail-length of GNRH1 mRNA and compromised the formation of translation initiation complex (TIC). Recently, we have shown that MKRN3 epigenetically regulates the transcription of GNRH1 through conjugating poly-Ub chains onto methyl-DNA bind protein 3 (MBD3). Therefore, MKRN3-mediated ubiquitin signalling could control both transcriptional and post-transcriptional switches of mammalian puberty initiation. While identifying MKRN3 as a novel tissue-specific translational regulator, our work also provided new mechanistic insights into the etiology of MKRN3 dysfunction-associated human CPP.
该敲除模型可用于：
- 研究PABPC4在泛素化介导的mRNA稳定性和翻译控制中的作用。
- 研究哺乳动物青春期的分子机制，特别是GNRH1 mRNA调控。
- 探索MKRN3依赖性信号通路在神经内分泌发育中的作用。
- 验证多聚A结合蛋白靶点在基因表达调控中的功能。
- 筛选生殖生物学背景下mRNA衰变或翻译的调节剂。
联系电话