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磷酸化ras基因相关蛋白Rab24抗体说明书

点击次数:102发布时间:2016/9/19 13:18:51

磷酸化ras基因相关蛋白Rab24抗体说明书

更新日期:2024/8/5 18:43:00

所 在 地:中国大陆

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品牌名称:上海雅吉

简单介绍:磷酸化ras基因相关蛋白Rab24抗体说明书性硬化症(tuberous sclerosis)又称结节性脑硬化,Bourneville病。本病可归类于神经皮肤综合征(亦称斑痣性错构瘤病),是源于外胚层的器官发育异常所致,病变累及神经系统、皮肤和眼,也可累及中胚层,内胚层器官如心、肺、骨,肾和胃肠等。皮脂腺瘤是皮肤神经末梢、增生的结缔组织和血管组成,视网膜可见胶质瘤、神经节细胞瘤,心、肾、肺、肝脏等也

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  公司介绍
为满足客户对抗目标靶标物单克隆抗体的迫切需求,单抗制备团队经过多年的系统深入研究,发现了磷酸化ras基因相关蛋白Rab24抗体说明书对杂交瘤形成与生长调节规律,提出了一种全新技术方案,通过探明人类干细胞因子bFGF、HFCS对目标多肽以及靶标蛋白阳性杂交瘤形成与生长调节规律,创建了杂交瘤细胞株半固体干细胞培养基-梯度筛选法(简称"两步筛选法"),突破了常规HAT、HT培养筛选法阳性率低、随机性大的局限。单克隆抗体制备服务*快可在100天内完成单抗制备过程,并且保证为客户提供2个阳性克隆以及高亲和力的抗体产品。
 
公司可根据客户的不同需要提供经济、快速而可靠的单克隆抗体制备的完整解决方案,本项技术服务包括:
  - Balb/c纯系小鼠免疫;
  - 脾细胞与SP2/0骨髓瘤细胞的融合;
  - 抗体产生细胞的ELISA筛选;
  - 抗体产生细胞的亚克隆与扩增;
  - 指定细胞克隆的体外培养或腹水瘤接种法生产单克隆抗体
产品特点
中文名称:磷酸化ras基因相关蛋白Rab24抗体说明书
别    名:TSC1(phospho S505); LAM; TSC1; Tuberous sclerosis 1 protein.
规格价格:0.1ml    
说 明 书:0.1ml  
产品类型:磷酸化抗体 
研究领域:肿瘤  免疫学  染色质和核信号  
抗体来源:Rabbit
克隆类型:Polyclonal
交叉反应:Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Horse, Rabbit, 
产品应用:WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 (石蜡切片需做抗原修复) 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量:128kDa
细胞定位:细胞浆 细胞膜 
性    状:Lyophilized or Liquid
浓    度:1mg/1ml
免 疫 原:KLH conjugated Synthesised phosphopeptide derived from human TSC1 around the phosphorylation site of Ser505 [FD(p-S)PF]
亚    型;IgG
纯化方法;affinity purified by Protein A
储 存 液;0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件;Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
PubMedPubMed
产品资料
产品介绍:background:
Hamartin, or TSC1, is a suspected tumor suppressor implicated in the disease tuberous sclerosis 1. It is a negative regulator of cell division controlling the transition from G0/G1 to S phase, and it seems to act through the phosphatidylinositol 3 kinase/Akt pathway. TSC1 interacts with tuberin m(TSC2), which is thought to be a GAP (GTPase Activating Protein) for the Rap1 and Rab5 small G Proteins. The Hamartin/Tuberin complex has been shown to inhibit mTor. Hamartin has also been shown to interact with ERM (Ezrin-Radixin-Moesin) proteins and with F-actin, suggesting a role for TSC proteins in modulation of cell adhesion and morphology.

Function:
In complex with TSC2, inhibits the nutrient-mediated or growth factor-stimulated phosphorylation of S6K1 and EIF4EBP1 by negatively regulating mTORC1 signaling. Seems not to be required for TSC2 GAP activity towards RHEB. Implicated as a tumor suppressor. Involved in microtubule-mediated protein transport, but this seems to be due to unregulated mTOR signaling.

Subunit:
Interacts with TSC2, leading to stabilize TSC2. In the absence of TSC2, TSC1 self-aggregates. Interacts with DOCK7. Interacts with FBXW5 and TBC1D7.

Subcellular Location:
Cytoplasm. Membrane; Peripheral membrane protein. Note=At steady state found in association with membranes.

Tissue Specificity:
Highly expressed in skeletal muscle, followed by heart, brain, placenta, pancreas, lung, liver and kidney. Also expressed in embryonic kidney cells.

Post-translational modifications:
Phosphorylation at Ser-505 does not affect interaction with TSC2. Phosphorylated upon DNA damage, probably by ATM or ATR.

DISEASE:
Defects in TSC1 are the cause of tuberous sclerosis type 1 (TSC1) [MIM:191100]. It is an autosomal dominant multi-system disorder that affects especially the brain, kidneys, heart, and skin. TS1C is characterized by hamartomas (benign overgrowths predominantly of a cell or tissue type that occurs normally in the organ) and hamartias (developmental abnormalities of tissue combination). Clinical symptoms can range from benign hypopigmented macules of the skin to profound mental retardation with intractable seizures to premature death from a variety of disease-associated causes. 
Defects in TSC1 may be a cause of focal cortical dysplasia of Taylor balloon cell type (FCDBC) [MIM:607341]. FCDBC is a subtype of cortical displasias linked to chronic intractable epilepsy. Cortical dysplasias display a broad spectrum of structural changes, which appear to result from changes in proliferation, migration, differentiation, and apoptosis of neuronal precursors and neurons during cortical development.

磷酸化ras基因相关蛋白Rab24抗体说明书Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 

    结节性硬化症为常染色体显性遗传,也常见散发病例。是肿瘤抑制基因,基因产物分别为Hamartin和tuberin,两者均调节细胞生长。
    结节性硬化症(tuberous sclerosis)又称结节性脑硬化,Bourneville病。本病可归类于神经皮肤综合征(亦称斑痣性错构瘤病),是源于外胚层的器官发育异常所致,病变累及神经系统、皮肤和眼,也可累及中胚层,内胚层器官如心、肺、骨,肾和胃肠等。皮脂腺瘤是皮肤神经末梢、增生的结缔组织和血管组成,视网膜可见胶质瘤、神经节细胞瘤,心、肾、肺、肝脏等也可发生肿瘤。
    而神经胶质增生性硬化结节广泛发生于大脑皮质、白质、基底节和室管膜下,常伴钙质沉积,可出现一位症及血管增生等,出现癫痫发作及智能减退为特征。

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