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。
SUV39H1 Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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- 实验流程
- 背景知识
Application 
| WB, E |
|---|---|
| Primary Accession | O43463 |
| Other Accession | NP_003164.1 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 47907 Da |
| Antigen Region | 79-108 aa |
| Gene ID | 6839 |
|---|---|
| Other Names | Histone-lysine N-methyltransferase SUV39H1, Histone H3-K9 methyltransferase 1, H3-K9-HMTase 1, Lysine N-methyltransferase 1A, Position-effect variegation 3-9 homolog, Suppressor of variegation 3-9 homolog 1, Su(var)3-9 homolog 1, SUV39H1, KMT1A, SUV39H |
| Target/Specificity | This SUV39H1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 79-108 amino acids from the N-terminal region of human SUV39H1. |
| 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 | SUV39H1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | SUV39H1 |
|---|---|
| Synonyms | KMT1A, SUV39H |
| Function | Histone methyltransferase that specifically trimethylates 'Lys-9' of histone H3 using monomethylated H3 'Lys-9' as substrate. Also weakly methylates histone H1 (in vitro). H3 'Lys-9' trimethylation represents a specific tag for epigenetic transcriptional repression by recruiting HP1 (CBX1, CBX3 and/or CBX5) proteins to methylated histones. Mainly functions in heterochromatin regions, thereby playing a central role in the establishment of constitutive heterochromatin at pericentric and telomere regions. H3 'Lys-9' trimethylation is also required to direct DNA methylation at pericentric repeats. SUV39H1 is targeted to histone H3 via its interaction with RB1 and is involved in many processes, such as repression of MYOD1-stimulated differentiation, regulation of the control switch for exiting the cell cycle and entering differentiation, repression by the PML-RARA fusion protein, BMP-induced repression, repression of switch recombination to IgA and regulation of telomere length. Component of the eNoSC (energy-dependent nucleolar silencing) complex, a complex that mediates silencing of rDNA in response to intracellular energy status and acts by recruiting histone-modifying enzymes. The eNoSC complex is able to sense the energy status of cell: upon glucose starvation, elevation of NAD(+)/NADP(+) ratio activates SIRT1, leading to histone H3 deacetylation followed by dimethylation of H3 at 'Lys-9' (H3K9me2) by SUV39H1 and the formation of silent chromatin in the rDNA locus. Recruited by the large PER complex to the E-box elements of the circadian target genes such as PER2 itself or PER1, contributes to the conversion of local chromatin to a heterochromatin-like repressive state through H3 'Lys-9' trimethylation. |
| Cellular Location | Nucleus. Nucleus lamina. Nucleus, nucleoplasm Chromosome, centromere. Note=Associates with centromeric constitutive heterochromatin |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
This gene is a member of the suppressor of variegation 3-9 homolog family and encodes a protein with a chromodomain and a C-terminal SET domain. This nuclear protein moves to the centromeres during mitosis and functions as a histone methyltransferase, methylating Lys-9 of histone H3. Overall, it plays a vital role in heterochromatin organization, chromosome segregation, and mitotic progression.
REFERENCES
Chen, L., et al. EMBO J. 29(15):2538-2552(2010)
Goyama, S., et al. Leukemia 24(1):81-88(2010)
Cherrier, T., et al. Oncogene 28(38):3380-3389(2009)
Li, Z., et al. J. Biol. Chem. 284(16):10361-10366(2009)
Spensberger, D., et al. FEBS Lett. 582(18):2761-2767(2008)
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