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Merck
CN

SAB3500022

Sigma-Aldrich

Anti-CEP164 antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

别名:

Anti-Centrosomal protein 164

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UNSPSC代码:
12352203
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生物来源

rabbit

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

buffered aqueous solution

种属反应性

mouse, human, rat

技术

immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable

NCBI登记号

UniProt登记号

运输

dry ice

储存温度

−20°C

基因信息

human ... CEP164(22897)

一般描述

CEP164 was initially identified as a centrosomal protein, but other studies have indicated that it also plays a role in the formation of primary cilia, the microtubule-based sensory antennae projecting from the surface of many eukaryotic cells as well as in DNA damage response acting as a mediator protein. CEP164 interacts with both ATR and ATM, proteins that trigger a number of cellular responses including the initiation of DNA damaged-induced cell cycle checkpoints. It is phosphorylated upon replication stress, ultraviolet (UV) radiation, and ionizing radiation; silencing of CEP164 significantly reduces the DNA damage-induced phosphorylation of several proteins in the DNA damage-activated signaling cascade and compromises cell survival after UV damage. At least two isoforms of CEP164 are known to exist.

免疫原

CEP164 antibody was raised against an 18 amino acid peptide near the amino terminus of human CEP164.

应用

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunofluorescence (1 paper)

特点和优势

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

外形

Supplied at approx. 1 mg/mL in phosphate buffered saline containing 0.02% sodium azide.

其他说明

The action of this antibody can be blocked using blocking peptide SBP3500022.

免责声明

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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储存分类代码

12 - Non Combustible Liquids

WGK

WGK 2

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

常规特殊物品
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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Chengbing Wang et al.
The Journal of biological chemistry, 288(41), 29518-29529 (2013-08-21)
The primary cilium is required for Hedgehog signaling. So far, all known ciliogenic proteins regulate Hedgehog signaling through their role in ciliogenesis. Here we show that the mouse DZIP1 regulates Hedgehog signaling through two mechanisms. First, DZIP1 interacts with GLI3
Claudio R Cortés et al.
Scientific reports, 6, 24083-24083 (2016-04-21)
Ciliopathies are a group of genetic disorders caused by defective assembly or dysfunction of the primary cilium, a microtubule-based cellular organelle that plays a key role in developmental signalling. Ciliopathies are clinically grouped in a large number of overlapping disorders
Hao Yan et al.
Nature communications, 11(1), 2196-2196 (2020-05-06)
Transition fibers (TFs) regulate cilia gating and make the primary cilium a distinct functional entity. However, molecular insights into the biogenesis of a functional cilia gate remain elusive. In a forward genetic screen in Caenorhabditis elegans, we uncover that TALP-3
Hao Lu et al.
Nature genetics, 49(7), 1025-1034 (2017-05-23)
Autosomal recessive polycystic kidney disease (ARPKD), usually considered to be a genetically homogeneous disease caused by mutations in PKHD1, has been associated with ciliary dysfunction. Here, we describe mutations in DZIP1L, which encodes DAZ interacting protein 1-like, in patients with
Chuan Chen et al.
Science advances, 7(26) (2021-06-25)
Mutation of ciliopathy protein HYLS1 causes the perinatal lethal hydrolethalus syndrome (HLS), yet the underlying molecular etiology and pathogenesis remain elusive. Here, we reveal unexpected mechanistic insights into the role of mammalian HYLS1 in regulating primary cilia. HYLS1 is recruited

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