- ￥2262
- LSM Bio
- 进口
- PAab06498
- 2025年07月15日
- ELISA,WB,IF,IP,FC
- E. coli - derived recombinant protein
- Human,Mouse ,Rat
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- 文献和实验
- 技术资料
- 免疫原：
protein kinase N2
- 亚型：
IgG
- 形态：
liquid
- 保存条件：
负20摄氏度
- 克隆性：
Polyclonal antibody
- 标记物：
Non-conjugated
- 适应物种：
Human,Mouse ,Rat
- 保质期：
6个月
- 抗原来源：
Rabbit
- 目录编号：
P67936
- 级别：
纯化级别
- 库存：
50
- 供应商：
LSM bio
- 宿主：
E. coli - derived recombinant protein
- 应用范围：
ELISA,WB,IF,IP,FC
- 浓度：
≥95% as determined by SDS-PAGE
- 靶点：
protein kinase N2
- 抗体英文名：
anti-PKN2 antibody,PKN2 antibody
- 抗体名：
anti-PKN2 抗体,PKN2 抗体
- 规格：
100μg
PKN2抗体| PKN2 antibody
货号 PAab06498
蛋白别名 PRK2 antibody, PRKCL2
蛋白介绍
PKC-related serine/threonine-protein kinase and Rho/Rac effector protein that participates in specific signal transduction responses in the cell. Plays a role in the regulation of cell cycle progression, actin cytoskeleton assembly, cell migration, cell adhesion, tumor cell invasion and transcription activation signaling processes. Phosphorylates CTTN in hyaluronan-induced astrocytes and hence decreases CTTN ability to associate with filamentous actin. Phosphorylates HDAC5, therefore lead to impair HDAC5 import. Direct RhoA target required for the regulation of the maturation of primordial junctions into apical junction formation in bronchial epithelial cells. Required for G2/M phases of the cell cycle progression and abscission during cytokinesis in a ECT2-dependent manner. Stimulates FYN kinase activity that is required for establishment of skin cell-cell adhesion during keratinocytes differentiation. Regulates epithelial bladder cells speed and direction of movement during cell migration and tumor cell invasion. Inhibits Akt pro-survival-induced kinase activity. Mediates Rho protein-induced transcriptional activation via the c- fos serum response factor (SRF). Phosphorylates HCV NS5B leading to stimulation of HCV RNA replication.
产品描述
anti-PKN2 antibody is a Rabbit Polyclonal antibody againstPKN2..
建议稀释比例
IHC
Western blot
(本抗体仅供体外科研用途，不可用于临床诊断!) "">
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文献和实验基因，其可通过IDR2结构域发生液-液相分离，在细胞核内形成凝聚体并结合NICD1激活Notch信号，调控心内膜内皮-间充质转化。团队发现室间隔缺损患者来源的Q401K突变会破坏MAML1相分离，抑制Notch活性；构建的Maml1 Q408K突变小鼠出现室间隔缺损、二叶式主动脉瓣等表型。机制上，PKN2通过磷酸化MAML1的S314位点抑制其相分离，发育关键期低表达PKN2维持MAML1凝聚体稳定以保障Notch信号传导。该研究首次建立MAML1相分离异常与先心病发病的关联，为阐明心内膜发育规律提供
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