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。
DCLRE1B Antibody (Center) 精选
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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- 实验流程
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Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | Q9H816 |
| Other Accession | NP_073747.1 |
| Reactivity | Human, Rat, Mouse |
| Predicted | Bovine, Canine, Rabbit |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 60002 Da |
| Antigen Region | 208-236 aa |
| Gene ID | 64858 |
|---|---|
| Other Names | 5' exonuclease Apollo, 31--, DNA cross-link repair 1B protein, SNM1 homolog B, SNMIB, hSNM1B, DCLRE1B, SNM1B |
| Target/Specificity | This DCLRE1B antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 208-236 amino acids from the Central region of human DCLRE1B. |
| Dilution | WB~~1:1000 IHC-P~~1:100~500 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 | DCLRE1B Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | DCLRE1B |
|---|---|
| Synonyms | SNM1B |
| Function | 5'-3' exonuclease that plays a central role in telomere maintenance and protection during S-phase. Participates in the protection of telomeres against non-homologous end-joining (NHEJ)- mediated repair, thereby ensuring that telomeres do not fuse. Plays a key role in telomeric loop (T loop) formation by being recruited by TERF2 at the leading end telomeres and by processing leading-end telomeres immediately after their replication via its exonuclease activity: generates 3' single-stranded overhang at the leading end telomeres avoiding blunt leading-end telomeres that are vulnerable to end-joining reactions and expose the telomere end in a manner that activates the DNA repair pathways. Together with TERF2, required to protect telomeres from replicative damage during replication by controlling the amount of DNA topoisomerase (TOP1, TOP2A and TOP2B) needed for telomere replication during fork passage and prevent aberrant telomere topology. Also involved in response to DNA damage: plays a role in response to DNA interstrand cross-links (ICLs) by facilitating double-strand break formation. In case of spindle stress, involved in prophase checkpoint. Possesses beta-lactamase activity, catalyzing the hydrolysis of penicillin G and nitrocefin (PubMed:31434986). Exhibits no activity towards other beta-lactam antibiotic classes including cephalosporins (cefotaxime) and carbapenems (imipenem) (PubMed:31434986). |
| Cellular Location | Chromosome, telomere. Nucleus. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Note=Mainly localizes to telomeres, recruited via its interaction with TERF2 During mitosis, localizes to the centrosome |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
DNA interstrand cross-links prevent strand separation, thereby physically blocking transcription, replication, and segregation of DNA. DCLRE1B is one of several evolutionarily conserved genes involved in repair of interstrand cross-links (Dronkert et al., 2000 [PubMed 10848582]).
REFERENCES
Anders, M., et al. Cell Cycle 8(11):1725-1732(2009) Liu, L., et al. Cell Cycle 8(4):628-638(2009) Freibaum, B.D., et al. J. Biol. Chem. 283(35):23671-23676(2008) Bae, J.B., et al. Oncogene 27(37):5045-5056(2008) Demuth, I., et al. DNA Repair (Amst.) 7(8):1192-1201(2008) Matsuoka, S., et al. Science 316(5828):1160-1166(2007) Lenain, C., et al. Curr. Biol. 16(13):1303-1310(2006) Freibaum, B.D., et al. J. Biol. Chem. 281(22):15033-15036(2006) Ishiai, M., et al. Mol. Cell. Biol. 24(24):10733-10741(2004) Demuth, I., et al. Oncogene 23(53):8611-8618(2004) Dronkert, M.L., et al. Mol. Cell. Biol. 20(13):4553-4561(2000)
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