SET Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application ![]()
| WB, IHC-P, E |
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Primary Accession | Q01105 |
Other Accession | Q63945, Q9EQU5, P53997, NP_001116293.1, NP_003002.2 |
Reactivity | Human |
Predicted | Drosophila, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 33489 Da |
Antigen Region | 47-75 aa |
Gene ID | 6418 |
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Other Names | Protein SET, HLA-DR-associated protein II, Inhibitor of granzyme A-activated DNase, IGAAD, PHAPII, Phosphatase 2A inhibitor I2PP2A, I-2PP2A, Template-activating factor I, TAF-I, SET |
Target/Specificity | This SET antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 47-75 amino acids from the N-terminal region of human SET. |
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 | SET Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | SET |
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Function | Multitasking protein, involved in apoptosis, transcription, nucleosome assembly and histone chaperoning. Isoform 2 anti-apoptotic activity is mediated by inhibition of the GZMA-activated DNase, NME1. In the course of cytotoxic T-lymphocyte (CTL)-induced apoptosis, GZMA cleaves SET, disrupting its binding to NME1 and releasing NME1 inhibition. Isoform 1 and isoform 2 are potent inhibitors of protein phosphatase 2A. Isoform 1 and isoform 2 inhibit EP300/CREBBP and PCAF- mediated acetylation of histones (HAT) and nucleosomes, most probably by masking the accessibility of lysines of histones to the acetylases. The predominant target for inhibition is histone H4. HAT inhibition leads to silencing of HAT-dependent transcription and prevents active demethylation of DNA. Both isoforms stimulate DNA replication of the adenovirus genome complexed with viral core proteins; however, isoform 2 specific activity is higher. |
Cellular Location | Cytoplasm, cytosol. Endoplasmic reticulum. Nucleus, nucleoplasm. Note=In the cytoplasm, found both in the cytosol and associated with the endoplasmic reticulum. The SET complex is associated with the endoplasmic reticulum. Following CTL attack and cleavage by GZMA, moves rapidly to the nucleus, where it is found in the nucleoplasm, avoiding the nucleolus. Similar translocation to the nucleus is also observed for lymphocyte-activated killer cells after the addition of calcium |
Tissue Location | Widely expressed. Low levels in quiescent cells during serum starvation, contact inhibition or differentiation. Highly expressed in Wilms' tumor |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Multitasking protein, involved in apoptosis, transcription, nucleosome assembly and histone binding. Isoform 2 anti-apoptotic activity is mediated by inhibition of the GZMA-activated DNase, NME1. In the course of cytotoxic T-lymphocyte (CTL)-induced apoptosis, GZMA cleaves SET, disrupting its binding to NME1 and releasing NME1 inhibition. Isoform 1 and isoform 2 are potent inhibitors of protein phosphatase 2A. Isoform 1 and isoform 2 inhibit EP300/CREBBP and PCAF-mediated acetylation of histones (HAT) and nucleosomes, most probably by masking the accessibility of lysines of histones to the acetylases. The predominant target for inhibition is histone H4. HAT inhibition leads to silencing of HAT-dependent transcription and prevents active demethylation of DNA. Both isoforms stimulate DNA replication of the adenovirus genome complexed with viral core proteins; however, isoform 2 specific activity is higher.
REFERENCES
Kim, D.W., et al. Biochem. Biophys. Res. Commun. 400(3):419-425(2010)
Chao, A., et al. Cancer Lett. 291(1):99-107(2010)
Jugessur, A., et al. PLoS ONE 5 (7), E11493 (2010) :
Samanta, A.K., et al. Oncogene 28(14):1669-1681(2009)
Kajiwara, Y., et al. PLoS ONE 4 (4), E5071 (2009) :

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