GEMIN2抗体GEMIN2兔多抗抗体Survival of
motor neuron protein-interacting protein 1 antibody抗体GEMIN2 Antibody, FITC conjugated抗体- ￥880 - 1320
- CUSABIO
- CN
- CSB-PA021329LC01HU
- 2025年07月09日
- /
- Rabbit
- Human
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- 详细信息
- 文献和实验
- 技术资料
- 免疫原：
Recombinant Human Gem-associated protein 2 protein (1-280AA)
- 亚型：
IgG
- 形态：
Liquid
- 保存条件：
Upon receipt, store at -20℃ or -80℃. Avoid repeated freeze.
- 克隆性：
Polyclonal
- 标记物：
FITC
- 适应物种：
Human
- 保质期：
6个月
- 抗原来源：
Homo sapiens (Human)
- 目录编号：
O14893
- 级别：
优
- 库存：
200
- 供应商：
武汉华美生物工程有限公司
- 宿主：
Rabbit
- 应用范围：
/
- 浓度：
>95%,Protein G purified
- 靶点：
GEMIN2
- 抗体英文名：
GEMIN2 Antibody, FITC conjugated
- 抗体名：
Survival of motor neuron protein-interacting protein 1 antibody
- 规格：
100μg/50μg
| 规格： | 100μg | 产品价格： | ￥1320.0 |
|---|---|---|---|
| 规格： | 50μg | 产品价格： | ￥880.0 |
保存缓冲液
Preservative: 0.03% Proclin 300Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
功能
The SMN complex plays a catalyst role in the assembly of small nuclear ribonucleoproteins (snRNPs), the building blocks of the spliceosome. Thereby, plays an important role in the splicing of cellular pre-mRNAs. Most spliceosomal snRNPs contain a common set of Sm proteins SNRPB, SNRPD1, SNRPD2, SNRPD3, SNRPE, SNRPF and SNRPG that assemble in a heptameric protein ring on the Sm site of the small nuclear RNA to form the core snRNP. In the cytosol, the Sm proteins SNRPD1, SNRPD2, SNRPE, SNRPF and SNRPG are trapped in an inactive 6S pICln-Sm complex by the chaperone CLNS1A that controls the assembly of the core snRNP. Dissociation by the SMN complex of CLNS1A from the trapped Sm proteins and their transfer to an SMN-Sm complex triggers the assembly of core snRNPs and their transport to the nucleus.风险提示：丁香通仅作为第三方平台，为商家信息发布提供平台空间。用户咨询产品时请注意保护个人信息及财产安全，合理判断，谨慎选购商品，商家和用户对交易行为负责。对于医疗器械类产品，请先查证核实企业经营资质和医疗器械产品注册证情况。
文献和实验：Transmembrane Protein GDE2 Induces Motor Neuron Differentiation in Vivo, Science , Vol 309, Issue 5744, 2212-2215 , 30 September 2005
Establishing In Vitro Models to Study Endogenous Neurotoxicants
aggregates in the trinucleotide repeat diseases (spinal bulbar muscular atrophy, Huntington’s disease, spinocerebellar ataxia 1 and 3, dentato-pallidoluysian atrophy) and cytoplasmic inclusions in familial and sporadic motor neuron diseases (45 ,46
. Keller‐Peck, C.R., Walsh, M.K., Gan, W.B., Feng, G., Sanes, J.R., and Lichtman, J.W. 2001. Asynchronous synapse elimination in neonatal motor units: Studies using GFP transgenic mice. Neuron 31:381‐394
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