MN1 Antibody (Center)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
---|---|
Primary Accession | Q10571 |
Other Accession | NP_002421.3 |
Reactivity | Human |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 136001 Da |
Antigen Region | 835-864 aa |
Gene ID | 4330 |
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Other Names | Probable tumor suppressor protein MN1, MN1 |
Target/Specificity | This MN1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 835-864 amino acids from the Central region of human MN1. |
Dilution | WB~~1:1000 |
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 | MN1 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | MN1 |
---|---|
Function | Transcriptional activator which specifically regulates expression of TBX22 in the posterior region of the developing palate. Required during later stages of palate development for growth and medial fusion of the palatal shelves. Promotes maturation and normal function of calvarial osteoblasts, including expression of the osteoclastogenic cytokine TNFSF11/RANKL. Necessary for normal development of the membranous bones of the skull (By similarity). May play a role in tumor suppression (Probable). |
Cellular Location | Nucleus. |
Tissue Location | Widely expressed in fetal and adult tissues. Highest expression is observed in fetal brain and skeletal muscle, and adult skeletal muscle. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Meningioma 1 (MN1) contains two sets of CAG repeats. It is disrupted by a balanced translocation (4;22) in a meningioma, and its inactivation may contribute to meningioma 32 pathogenesis.
References
Liu, T., et al. Leukemia 24(3):601-612(2010)
Kandilci, A., et al. Blood 114(8):1596-1606(2009)
Trynka, G., et al. Gut 58(8):1078-1083(2009)
Langer, C., et al. J. Clin. Oncol. 27(19):3198-3204(2009)
Schroeder, T., et al. Leuk. Lymphoma 50(6):1043-1046(2009)
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