L-Myc (E3M5P) Rabbit mAb #76266
- WB
- IP
- ChIP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 62 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- ChIP-Chromatin Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
For optimal ChIP results, use 10 μl of antibody and 10 μg of chromatin (approximately 4 × 106 cells) per IP. This antibody has been validated using SimpleChIP® Enzymatic Chromatin IP Kits.
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:200 |
| Chromatin IP | 1:50 |
Storage
Protocol
Specificity / Sensitivity
L-Myc (E3M5P) Rabbit mAb recognizes endogenous levels of total L-Myc protein. Cross-reactivity was not observed with other family members.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the carboxy terminus of human L-Myc protein. The epitope has been mapped to residues surrounding Thr190.
Background
Members of the Myc/Max/Mad network function as transcriptional regulators with roles in various aspects of cell behavior, including proliferation, differentiation, and apoptosis (1). These proteins share a common basic-helix-loop-helix leucine zipper (bHLH-ZIP) motif required for dimerization and DNA-binding. Max was originally discovered based on its ability to associate with c-Myc and found to be required for the ability of Myc to bind DNA and activate transcription (2). Subsequently, Max has been viewed as a central component of the transcriptional network, forming homodimers as well as heterodimers with other members of the Myc and Mad families (1). The association between Max and either Myc or Mad can have opposing effects on transcriptional regulation and cell behavior (1). The Mad family consists of four related proteins; Mad1, Mad2 (Mxi1), Mad3, and Mad4, and the more distantly related members of the bHLH-ZIP family, Mnt and Mga. Like Myc, the Mad proteins are tightly regulated with short half-lives. In general, Mad family members interfere with Myc-mediated processes, such as proliferation, transformation, and prevention of apoptosis by inhibiting transcription (3,4).
The Myc family is comprised of c-Myc, N-Myc, and L-Myc with often distinct patterns of expression during development as well as cancer (5). Amplification of each of the family members in cancer is frequently mutually exclusive with c-Myc being the most widely studied and most commonly amplified. N-Myc amplification, on the other hand, is found predominantly in neuroblastomas, and L-Myc amplification has been described in small cell lung cancer (SCLC) (6). Amplification of L-Myc in SCLC may result from chromosomal rearrangement between the rlf and MYCL genes (7). L-Myc expression by dendritic cells may be required for optimal T cell priming (8).
- Baudino, T.A. and Cleveland, J.L. (2001) Mol Cell Biol 21, 691-702.
- Blackwood, E.M. and Eisenman, R.N. (1991) Science 251, 1211-7.
- Henriksson, M. and Lüscher, B. (1996) Adv Cancer Res 68, 109-82.
- Grandori, C. et al. (2000) Annu Rev Cell Dev Biol 16, 653-99.
- Nesbit, C.E. et al. (1999) Oncogene 18, 3004-16.
- Nau, M.M. et al. Nature 318, 69-73.
- Mäkelä, T.P. et al. (1991) EMBO J 10, 1331-5.
- KC, W. et al. (2014) Nature 507, 243-7.
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