RAI17/ZMIZ1 (E2X3X) Rabbit mAb #89500
- WB
- IP
- IHC
Supporting Data
| REACTIVITY | H M Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 120, 130 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| Immunohistochemistry (Paraffin) | 1:100 - 1:400 |
Storage
Protocol
Specificity / Sensitivity
RAI17/ZMIZ1 (E2X3X) Rabbit mAb recognizes endogenous levels of total RAI17/ZMIZ1 protein.
Species Reactivity:
Human, Mouse, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro902 of human RAI17/ZMIZ1 protein.
Background
ZMIZ1, also known as ZIMP10 or RAI17, is a member of the Protein Inhibitor of Activated STAT (PIAS)-like family of transcriptional coregulators (1). ZMIZ1 was initially discovered as a novel coregulator of the androgen receptor (AR) and was shown to augment AR activity by enhancing sumoylation of the receptor (2). Subsequent studies have shown that ZMIZ1 can also act as a transcriptional coactivator of p53 (3) and SMAD3 (4). During thymopoiesis, ZMIZ1 was shown to promote pre-T-cell proliferation through cooperative induction of a subset of NOTCH target genes (5). In T-cell acute lymphoblastic leukemia (T-ALL) cells, ZMIZ1 was shown to engage directly with NOTCH1 through an N-terminal tetratricopeptide repeat (TPR) domain, facilitating its recruitment to a long-range acting enhancer element to promote MYC transcription and activity. Moreover, inhibition of ZMIZ1 impaired the initiation and maintenance of NOTCH-induced T-ALL (6). Although NOTCH1 appears to rely on ZMIZ1 to selectively amplify an oncogenic subset of target genes, research studies suggest ZMIZ1 is not involved in NOTCH-mediated intestinal homeostasis or myeloid suppression, suggesting that therapeutic strategies targeting ZMIZ1 may provide an opportunity to indirectly target NOTCH-driven cancers, with reduced adverse effects (7).
Limited Uses
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