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安全信息

SAB4502958

Sigma-Aldrich

抗-TGF β 受体I 兔抗

affinity isolated antibody

别名:

ADRB2, ALK-5, ESK2, SKR4, 激活素受体样激酶5

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About This Item

UNSPSC代码:
12352203
NACRES:
NA.41

生物来源

rabbit

质量水平

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

形式

buffered aqueous solution

分子量

antigen 55 kDa

种属反应性

mouse, human, rat

浓度

~1 mg/mL

技术

ELISA: 1:10000
immunofluorescence: 1:100-1:500
western blot: 1:500-1:1000

NCBI登记号

UniProt登记号

运输

wet ice

储存温度

−20°C

靶向翻译后修饰

unmodified

基因信息

human ... TGFBR1(7046)

相关类别

一般描述

抗-TGF β受体I抗体可检测内源性总TGF β受体I蛋白水平。
转化生长因子β受体-1 (TGF-β R1),也称为激活素受体样激酶5(ALK5)受体,由人类染色体9q22.3上的基因编码。在人类组织中广泛表达。

免疫原

该抗血清是靶向人TGFβ受体I合成肽制备的。

免疫原范围:131-180

应用

兔抗-TGF-β受体I抗体已用于免疫组化。
  • 免疫组织化学
  • 蛋白质印迹
  • 免疫荧光

生化/生理作用

转化生长因子β 受体-1 (TGF-β R1)增进肺成纤维细胞中胶原蛋白的生成,在碳纳米管诱导的纤维发生中起着至关重要的作用。 TβR依赖性信号在细胞生长和分化中起关键作用,TGF-β R1 的多态性或突变导致头颈癌。 激活素受体样激酶5(ALK5)或 TGF-β R1 促进Smad 2 (small mothers against decapentaplegic) 和Smad3 的磷酸化。活化的ALK5 抑制内皮细胞(EC)的迁移和增殖。ALK1可用作ALK5/Smad信号传导的拮抗剂。TGF-βR1 的突变也可导致名为多发性自愈性鳞状上皮瘤(MSSE)或Ferguson-Smith 病(FSD)的常染色体显性皮肤癌。

特点和优势

您可完全放心的评估我们的抗体。如果抗体在您的应用中没有发挥效果,我们将给予您全额赔偿或更换抗体。了解更多。

外形

兔IgG,溶于磷酸盐缓冲盐水(不含Mg2+和Ca2+),pH7.4,150mM NaCl,0.02%叠氮化钠和50%甘油中。

免责声明

除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、体外或体内治疗用途,或人类或动物任何类型的消费或使用。

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WGK

nwg

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

常规特殊物品

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Rongfen Gao et al.
Oxidative medicine and cellular longevity, 2023, 5012474-5012474 (2023-02-15)
Both epithelial-to-mesenchymal (EMT) and endothelial-to-mesenchymal (EndMT) transitions have shown to contribute to the development and progression of kidney fibrosis. It has been reported that apelin, a regulatory peptide, alleviates EMT by inhibiting the transforming growth factor β (TGFβ) pathway in
Wenlong Yang et al.
Journal of molecular and cellular cardiology, 134, 119-130 (2019-07-13)
Trimethylamine N-oxide (TMAO), a gut microbe-derived metabolite of dietary choline and other trimethylamine-containing nutrients, has been associated with poor prognosis in coronary heart disease. However, the role and underlying mechanisms of TMAO in the cardiac fibrosis after myocardial infarction (MI)
Feng Zhang et al.
BMC medical genomics, 17(1), 56-56 (2024-02-21)
Liver fibrosis is a major global healths problem; nevertheless, its molecular mechanism are not completely clear. This study aimed to build a lncRNA-miRNA-mRNA network, identify potentially related lncRNAs, and explore the pathogenesis of liver fibrosis. We used the Gene Expression
T J Knobloch et al.
Mutation research, 479(1-2), 131-139 (2001-07-27)
Transforming growth factor-beta receptor (TbetaR)-dependent signals are critical for cell growth and differentiation and are often disrupted during tumorigenesis. The entire coding region of TbetaR-I and flanking intron sequences from 30 head and neck carcinomas were examined for alterations using
Marie José Goumans et al.
Molecular cell, 12(4), 817-828 (2003-10-29)
Transforming growth factor-beta (TGFbeta) regulates the activation state of the endothelium via two opposing type I receptor/Smad pathways. Activin receptor-like kinase-1 (ALK1) induces Smad1/5 phosphorylation, leading to an increase in endothelial cell proliferation and migration, while ALK5 promotes Smad2/3 activation

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