癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
ERCC5 Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, E |
|---|---|
| Primary Accession | P28715 |
| Other Accession | NP_000114.2 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 133108 Da |
| Antigen Region | 1151-1178 aa |
| Gene ID | 2073 |
|---|---|
| Other Names | DNA repair protein complementing XP-G cells, 31--, DNA excision repair protein ERCC-5, Xeroderma pigmentosum group G-complementing protein, ERCC5, ERCM2, XPG, XPGC |
| Target/Specificity | This ERCC5 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1151-1178 amino acids from the C-terminal region of human ERCC5. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | ERCC5 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ERCC5 |
|---|---|
| Synonyms | ERCM2, XPG, XPGC |
| Function | Single-stranded structure-specific DNA endonuclease involved in DNA excision repair (PubMed:32522879, PubMed:32821917, PubMed:7651464, PubMed:8078765, PubMed:8090225, PubMed:8206890). Makes the 3'incision in DNA nucleotide excision repair (NER) (PubMed:32522879, PubMed:32821917, PubMed:8078765, PubMed:8090225). Binds and bends DNA repair bubble substrate and breaks base stacking at the single-strand/double-strand DNA junction of the DNA bubble (PubMed:32522879). Plays a role in base excision repair (BER) by promoting the binding of DNA glycosylase NTHL1 to its substrate and increasing NTHL1 catalytic activity that removes oxidized pyrimidines from DNA (PubMed:9927729). Involved in transcription-coupled nucleotide excision repair (TCR) which allows RNA polymerase II-blocking lesions to be rapidly removed from the transcribed strand of active genes (PubMed:16246722). Functions during the initial step of TCR in cooperation with ERCC6/CSB to recognized stalled RNA polymerase II (PubMed:16246722). Also, stimulates ERCC6/CSB binding to the DNA repair bubble and ERCC6/CSB ATPase activity (PubMed:16246722). Required for DNA replication fork maintenance and preservation of genomic stability (PubMed:26833090, PubMed:32522879). Involved in homologous recombination repair (HRR) induced by DNA replication stress by recruiting RAD51, BRCA2, and PALB2 to the damaged DNA site (PubMed:26833090). In TFIIH stimulates the 5'-3' helicase activity of XPD/ERCC2 and the DNA translocase activity of XPB/ERCC3 (PubMed:31253769). During HRR, binds to the replication fork with high specificity and stabilizes it (PubMed:32522879). Also, acts upstream of HRR, to promote the release of BRCA1 from DNA (PubMed:26833090). |
| Cellular Location | Nucleus. Chromosome. Note=Colocalizes with RAD51 to nuclear foci in S phase (PubMed:26833090). Localizes to DNA double-strand breaks (DBS) during replication stress (PubMed:26833090). Colocalizes with BRCA2 to nuclear foci following DNA replication stress (PubMed:26833090). |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Excision repair cross-complementing rodent repair deficiency, complementation group 5 (xeroderma pigmentosum, complementation group G) is involved in excision repair of UV-induced DNA damage. Mutations cause Cockayne syndrome, which is characterized by severe growth defects, mental retardation, and cachexia. Multiple alternatively spliced transcript variants encoding distinct isoforms have been described, but the biological validity of all variants has not been determined. [provided by RefSeq].
REFERENCES
Figl, A., et al. Mutat. Res. 702(1):8-16(2010)
Ho-Pun-Cheung, A., et al. Pharmacogenomics J. (2010) In press :
Briggs, F.B., et al. Am. J. Epidemiol. 172(2):217-224(2010)
Monsees, G.M., et al. Breast Cancer Res. Treat. (2010) In press :
Canbay, E., et al. Anticancer Res. 30(4):1359-1364(2010)
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