FITC标记的DNA补充修复XPC细胞蛋白抗体上海沪震实业有限公司

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产品名称: FITC标记的DNA补充修复XPC细胞蛋白抗体
英文名称: Anti-XPC/FITC
抗体货号: HZ-6634R-FITC
产品规格: 100ul
级    别: 分析纯, , 分析纯,
产品产地: 中国/上海
品牌商标: HZbscience
价    格: 2980元
抗原: Rabbit
抗原来源: Rabbit
抗体来源: Rabbit
适用物种: 
FITCconjugate:FITC
应用范围: IF=1:50-200
更新时间: 2018/7/13 9:03:00
详细资料:  实验方法技术资料
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使用范围:仅限科研使用,不能应用于临床
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产品详细描述

 Rabbit Anti-XPC/FITC Conjugated antibody

FITC标记的DNA补充修复XPC细胞蛋白抗体

 

英文名称 Anti-XPC/FITC
中文名称 FITC标记的DNA补充修复XPC细胞蛋白抗体
别    名 Xeroderma pigmentosum complementation group C; DNA repair protein complementing XP C cells; DNA repair protein complementing XP-C cells; DNA repair protein complementing XPC cells; p125; RAD4; Xeroderma pigmentosum group C complementing protein; Xeroderma pigmentosum group C protein; Xeroderma pigmentosum group C-complementing protein; Xeroderma pigmentosum group III; XP 3; XP C; XP group C; XP3; Xpc; XPC gene; XPC_HUMAN; XPCC.  
规格价格 100ul/2980元 购买        大包装/询价
说 明 书 100ul  
研究领域 细胞生物  表观遗传学  
抗体来源 Rabbit
克隆类型 Polyclonal
交叉反应 Human, Mouse, Rat, Dog, Pig, Cow, Horse, Guinea Pig, 
产品应用 IF=1:50-200  
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 106kDa
性    状 Lyophilized or Liquid
浓    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human Xeroderma pigmentosum group C
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.
产品介绍 background:
The XPC complex is proposed to represent the first factor bound at the sites of DNA damage and together with other core recognition factors, XPA, RPA and the TFIIH complex, is part of the pre-incision (or initial recognition) complex. The XPC complex recognizes a wide spectrum of damaged DNA characterized by distortions of the DNA helix such as single-stranded loops, mismatched bubbles or single stranded overhangs. The orientation of XPC complex binding appears to be crucial for inducing a productive NER. XPC complex is proposed to recognize and to interact with unpaired bases on the undamaged DNA strand which is followed by recruitment of the TFIIH complex and subsequent scanning for lesions in the opposite strand in a 5'-to-3' direction by the NER machinery. Cyclobutane pyrimidine dimers (CPDs) which are formed upon UV-induced DNA damage esacpe detection by the XPC complex due to a low degree of structural perurbation. Instead they are detected by the UV-DDB complex which in turn recruits and cooperates with the XPC complex in the respective DNA repair. In vitro, the XPC:RAD23B dimer is sufficient to initiate NER; it preferentially binds to cisplatin and UV-damaged double-stranded DNA and also binds to a variety of chemically and structurally diverse DNA adducts. XPC:RAD23B contacts DNA both 5' and 3' of a cisplatin lesion with a preference for the 5' side. XPC:RAD23B induces a bend in DNA upon binding. XPC:RAD23B stimulates the activity of DNA glycosylases TDG and SMUG1.

Function:
Involved in global genome nucleotide excision repair (GG-NER) by acting as damage sensing and DNA-binding factor component of the XPC complex. Has only a low DNA repair activity by itself which is stimulated by RAD23B and RAD23A. Has a preference to bind DNA containing a short single-stranded segment but not to damaged oligonucleotides. This feature is proposed to be related to a dynamic sensor function: XPC can rapidly screen duplex DNA for non-hydrogen-bonded bases by forming a transient nucleoprotein intermediate complex which matures into a stable recognition complex through an intrinsic single-stranded DNA-binding activity. 
The XPC complex is proposed to represent the first factor bound at the sites of DNA damage and together with other core recognition factors, XPA, RPA and the TFIIH complex, is part of the pre-incision (or initial recognition) complex. The XPC complex recognizes a wide spectrum of damaged DNA characterized by distortions of the DNA helix such as single-stranded loops, mismatched bubbles or single stranded overhangs. The orientation of XPC complex binding appears to be crucial for inducing a productive NER. XPC complex is proposed to recognize and to interact with unpaired bases on the undamaged DNA strand which is followed by recruitment of the TFIIH complex and subsequent scanning for lesions in the opposite strand in a 5'-to-3' direction by the NER machinery. Cyclobutane pyrimidine dimers (CPDs) which are formed upon UV-induced DNA damage esacpe detection by the XPC complex due to a low degree of structural perurbation. Instead they are detected by the UV-DDB complex which in turn recruits and cooperates with the XPC complex in the respective DNA repair. In vitro, the XPC:RAD23B dimer is sufficient to initiate NER; it preferentially binds to cisplatin and UV-damaged double-stranded DNA and also binds to a variety of chemically and structurally diverse DNA adducts. XPC:RAD23B contacts DNA both 5' and 3' of a cisplatin lesion with a preference for the 5' side. XPC:RAD23B induces a bend in DNA upon binding. XPC:RAD23B stimulates the activity of DNA glycosylases TDG and SMUG1. 

Subunit:
Component of the XPC complex composed of XPC, RAD23B and CETN2. Interacts with RAD23A; the interaction is suggesting the existence of a functional equivalent variant XPC complex. Interacts with TDG; the interaction is demonstrated using the XPC:RAD23B dimer. Interacts with SMUG1; the interaction is demonstrated using the XPC:RAD23B dimer. Interacts with DDB2. Interacts with CCNH, GTF2H1 and ERCC3.

Subcellular Location:
Nucleus. Cytoplasm. Note=Omnipresent in the nucleus and consistently associates with and dissociates from DNA in the absence of DNA damage. Continuously shuttles between the cytoplasm and the nucleus, which is impeded by the presence of NER lesions.

DISEASE:
Defects in XPC are a cause of xeroderma pigmentosum complementation group C (XP-C) [MIM:278720]; also known as xeroderma pigmentosum III (XP3). XP-C is a rare human autosomal recessive disease characterized by solar sensitivity, high predisposition for developing cancers on areas exposed to sunlight and, in some cases, neurological abnormalities. 

Similarity:
Belongs to the XPC family.

Database links:

Entrez Gene: 7508 Human

Entrez Gene: 22591 Mouse

Entrez Gene: 312560 Rat

Omim: 613208 Human

SwissProt: Q01831 Human

SwissProt: P51612 Mouse

Unigene: 475538 Human

Unigene: 2806 Mouse

Unigene: 22820 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications
   

XPC复合物被提出来代表DNA损伤部位的第一因子结合,并与其他核心识别因子XPA、RPA和TFIIH复合物一起,是预切割(或初始识别)复合物的一部分。XPC复合体识别了DNA DNA的扭曲谱,其特征在于DNA螺旋的扭曲,如单链环、错配气泡或单链悬垂。XPC复合结合的方向似乎是诱导生产性NER的关键。XPC复合物被提出识别和与未成对碱基相互作用,在未损伤的DNA链上,随后通过招募TFIIH复合物,随后通过NER机械在5’-3’方向对相反的链中的病变进行扫描。Cyclobutane pyrimidine dimers(CPDS)是由于紫外线引起的DNA损伤ESCAPE检测的XPC络合物由于低程度的结构均势。相反,它们是由UV-DDB复合体检测的,这反过来又在各自的DNA修复中招募并配合XPC复合体。在体外,XPC:RAD23 B二聚体足以启动NER;它优先结合顺铂和UV损伤的双链DNA,并且还结合多种化学和结构上不同的DNA加合物。XPC:RAD23 B接触顺铂病变的5’和3’DNA,偏爱5’侧。XPC:RAD23 B在结合后诱导DNA的弯曲。XPC:RAD23 B刺激DNA糖基化酶TDG和SMGU1的活性。

生物在线声明:以上所展示的信息由企业自行提供,内容的真实性、准确性和合法性由发布企业负责。生物在线对此不承担任何保证责任。

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