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。
MSL2 Antibody (N-term) 精选
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, E |
|---|---|
| Primary Accession | Q9HCI7 |
| Other Accession | Q69ZF8, NP_001138889.1, NP_060603.2 |
| Reactivity | Human |
| Predicted | Mouse, Rat, Bovine, Canine, Rabbit, Chicken |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 62541 Da |
| Antigen Region | 4-32 aa |
| Gene ID | 55167 |
|---|---|
| Other Names | E3 ubiquitin-protein ligase MSL2, 632-, Male-specific lethal 2-like 1, MSL2-like 1, Male-specific lethal-2 homolog, MSL-2, Male-specific lethal-2 homolog 1, RING finger protein 184, MSL2, KIAA1585, MSL2L1, RNF184 |
| Target/Specificity | This MSL2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 4-32 amino acids from the N-terminal region of human MSL2. |
| 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 | MSL2 Antibody (N-term) 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 | MSL2 {ECO:0000303|PubMed:16227571, ECO:0000312|HGNC:HGNC:25544} |
|---|---|
| Function | Non-catalytic component of the MSL histone acetyltransferase complex, a multiprotein complex that mediates the majority of histone H4 acetylation at 'Lys-16' (H4K16ac), an epigenetic mark that prevents chromatin compaction (PubMed:16543150, PubMed:33837287). The MSL complex is required for chromosome stability and genome integrity by maintaining homeostatic levels of H4K16ac (PubMed:33837287). The MSL complex is also involved in gene dosage by promoting up-regulation of genes expressed by the X chromosome (By similarity). X up-regulation is required to compensate for autosomal biallelic expression (By similarity). The MSL complex also participates in gene dosage compensation by promoting expression of Tsix non-coding RNA (By similarity). MSL2 plays a key role in gene dosage by ensuring biallelic expression of a subset of dosage-sensitive genes, including many haploinsufficient genes (By similarity). Acts by promoting promoter- enhancer contacts, thereby preventing DNA methylation of one allele and creating a methylation-free environment for methylation-sensitive transcription factors such as SP1, KANSL1 and KANSL3 (By similarity). Also acts as an E3 ubiquitin ligase that promotes monoubiquitination of histone H2B at 'Lys-35' (H2BK34Ub), but not that of H2A (PubMed:21726816, PubMed:30930284). This activity is greatly enhanced by heterodimerization with MSL1 (PubMed:21726816, PubMed:30930284). H2B ubiquitination in turn stimulates histone H3 methylation at 'Lys-4' (H3K4me) and 'Lys-79' (H3K79me) and leads to gene activation, including that of HOXA9 and MEIS1 (PubMed:21726816). Also involved in the DNA damage response by mediating ubiquitination of TP53/p53 and TP53BP1 (PubMed:19033443, PubMed:23874665). |
| Cellular Location | Nucleus. Chromosome. Note=Associates with both promoters and enhancers of target genes, maintaining promoter-enhancer contacts {ECO:0000250|UniProtKB:Q69ZF8} |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Component of histone acetyltransferase complex responsible for the majority of histone H4 acetylation at lysine 16 which is implicated in the formation of higher-order chromatin structure.
REFERENCES
Dehghan, A., et al. Circ Cardiovasc Genet 2(2):125-133(2009)
Mendjan, S., et al. Mol. Cell 21(6):811-823(2006)
Smith, E.R., et al. Mol. Cell. Biol. 25(21):9175-9188(2005)
Marin, I. J. Mol. Evol. 56(5):527-539(2003)
Lyman, L.M., et al. Genetics 147(4):1743-1753(1997)
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