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Merck
CN

MABT95

抗-Arp2/3复合抗体,克隆13C9

clone 13C9, from mouse

别名:

Actin-related protein 2/3 complex subunit 3, Arp2/3 complex 21 kDa subunit, p21-ARC

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
13C9, monoclonal
Application:
immunohistochemistry
western blot
Species reactivity:
human
Citations:
8
Technique(s):
immunohistochemistry: suitable (paraffin)
western blot: suitable
Uniprot accession no.:
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产品名称

抗-Arp2/3复合抗体,克隆13C9, clone 13C9, from mouse

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

13C9, monoclonal

species reactivity

human

technique(s)

immunohistochemistry: suitable (paraffin)
western blot: suitable

isotype

IgG2aκ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... ARPC3(10094)

Analysis Note

对照
MCF-7细胞裂解物
通过蛋白质印迹法在MCF-7细胞裂解物中进行评估。

蛋白质印迹分析: 该抗体以1:5,000稀释度在10 µg MCF-7细胞裂解物上检测到Arp2/3复合物。

Application

免疫组织化学分析: 一个代表性批次以1:5,000稀释度在人结肠直肠癌和人结肠组织中检测到Arp2/3复合物(如果染色太强,抗体可能需要进一步稀释 - 最佳稀释度无法由最终用户确定)。
抗Arp2/3复合物抗体,克隆13C9检测Arp2/3复合物的水平,&已发布&验证可用于WB、IH(P)。
研究子类别
细胞骨架
研究类别
细胞结构

Disclaimer

除非我们的目录或产品随附的其他公司文件中另有说明,否则我们的产品预期仅用于研究用途,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、离体或体内治疗用途或对人类或动物的任何类型的消费或应用。

General description

包含ARP2、ARP3、ARPC1B/p41-ARC、ARPC2/p34-ARC、ARPC3/p21-ARC、ARPC4/p20-ARC和ARPC5/p16-ARC的ARP2/3复合物在调节细胞骨架中的肌动蛋白聚合。七个亚基的复合′物中的两个(ARP2和ARP3)与单体肌动蛋白非常相似,并充当新肌动蛋白丝的成核位点。Arp2/3复合物与活化成核促进因子(NPF)协同工作,以帮助形成分支肌动蛋白网络。肌动蛋白细胞骨架重组的调节对于脂质囊泡的细胞迁移、吞噬作用和细胞内运动等过程很重要。
观测分子量〜20 kDa

Immunogen

GST标记的重组蛋白对应于人Arp2/3复合物。

Physical form

形式:纯化
纯化的小鼠单克隆IgG2aκ,溶于含0.1 M Tris-甘氨酸(pH 7.4)、150 mM NaCl和0.05%叠氮化钠的缓冲液中。
纯化蛋白G

Preparation Note

自接收之日起,在2-8°C下可稳定保存1年。

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存储类别

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Miran Rada et al.
Cancers, 14(5) (2022-03-11)
Vessel co-option is correlated with resistance against anti-angiogenic therapy in colorectal cancer liver metastases (CRCLM). Vessel co-opting lesions are characterized by highly motile cancer cells that move toward and along the pre-existing vessels in the surrounding nonmalignant tissue and co-opt
Miran Rada et al.
Cancers, 14(10) (2022-05-29)
Resistance to anti-angiogenic therapy is a major challenge in the treatment of colorectal cancer liver metastases (CRCLMs). Vessel co-option has been identified as a key contributor to anti-angiogenic therapy resistance in CRCLMs. Recently, we identified a positive correlation between the
Sophia Frentzas et al.
Nature medicine, 22(11), 1294-1302 (2016-11-01)
The efficacy of angiogenesis inhibitors in cancer is limited by resistance mechanisms that are poorly understood. Notably, instead of through the induction of angiogenesis, tumor vascularization can occur through the nonangiogenic mechanism of vessel co-option. Here we show that vessel
Diana C Muñoz-Lasso et al.
Scientific reports, 10(1), 5207-5207 (2020-04-07)
Abnormalities in actin cytoskeleton have been linked to Friedreich's ataxia (FRDA), an inherited peripheral neuropathy characterised by an early loss of neurons in dorsal root ganglia (DRG) among other clinical symptoms. Despite all efforts to date, we still do not
Aida M Lopez-Guerrero et al.
Scientific reports, 10(1), 6580-6580 (2020-04-22)
Tumor invasion requires efficient cell migration, which is achieved by the generation of persistent and polarized lamellipodia. The generation of lamellipodia is supported by actin dynamics at the leading edge where a complex of proteins known as the WAVE regulatory

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