SNAP25基因敲除HEK293细胞

SNAP25基因敲除HEK293细胞
货号:

EDJ-KQ5807

物种:

细胞名称:

HEK293

基因名称:

SNAP25

基因ID:

6616

规格:

1×10⁶cells

SNAP25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-KQ5807
产品名称 SNAP25 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 SNAP25
基因ID
基因别名 CMS18|DEE117|RIC-4|RIC4|SEC9|SNAP|SNAP-25|SUP|bA416N4.2|dJ1068F16.2
摘要
Synaptic vesicle membrane docking and fusion is mediated by SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) located on the vesicle membrane (v-SNAREs) and the target membrane (t-SNAREs). The assembled v-SNARE/t-SNARE complex consists of a bundle of four helices, one of which is supplied by v-SNARE and the other three by t-SNARE. For t-SNAREs on the plasma membrane, the protein syntaxin supplies one helix and the protein encoded by this gene contributes the other two. Therefore, this gene product is a presynaptic plasma membrane protein involved in the regulation of neurotransmitter release. Two alternative transcript variants encoding different protein isoforms have been described for this gene. [provided by RefSeq, Jul 2008]
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
Allele1Allele2Allele1 Allele2
AmelogeninXX
CSF1P0121112
D2S13381919
D3S135815171517
D5S818889
D7S82011121112
D8S117912141214
D13S31712141214
D16S539913913
D18S5117181718
D19S43315181518
D21S112830.22830.2
FGA2323
Penta D910910
Penta E715715
TH0179.379.3
TPOX1111
vWA16191619
D6S10431111
D12S39119211115
D2S44111151115
* 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。
* 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

IF=15
Neuron
SNARE (soluble N-ethylmaleimide sensitive factor attachment protein receptor) complex, composed of synaptobrevin, syntaxin, and SNAP25, forms the essential fusion machinery for neurotransmitter release. Recent studies have reported several mutations in the gene encoding SNAP25 as a causative factor for developmental and epileptic encephalopathies of infancy and childhood with diverse clinical manifestations. However, it remains unclear how SNAP25 mutations give rise to these disorders. Here, we show that although structurally clustered mutations in SNAP25 give rise to related synaptic transmission phenotypes, specific alterations in spontaneous neurotransmitter release are a key factor to account for disease heterogeneity. Importantly, we identified a single mutation that augments spontaneous release without altering evoked release, suggesting that aberrant spontaneous release is sufficient to cause disease in humans.
该敲除模型可用于: - 研究SNAP25在异常自发性神经传递中的作用。 - 模拟SNAP25相关脑病及相关神经系统疾病。 - 研究突触囊泡胞吐和神经递质释放机制。 - 评估靶向突触功能障碍的治疗干预措施。 - 探索SNAP25缺乏模型中的基因型-表型相关性。

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