Cell Signaling Technology
XP Monoclonal Antibody

Product Pathways - Apoptosis / Autophagy

c-Myc (D84C12) XP® Rabbit mAb #5605

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP IF-IC F H M R (Mk) (Dg) (Pg) Endogenous 57-65 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IF-IC=Immunofluorescence (Immunocytochemistry)  F=Flow Cytometry
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey  Dg=Dog  Pg=Pig
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

c-Myc (D84C12) XP® Rabbit mAb detects endogenous levels of total c-Myc protein. This antibody is not recommended for detection of Myc-tagged fusion proteins (use Cell Signaling Technology cat. #2276 or #2278).

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to amino-terminal residues of c-Myc.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, mock transfected or transfected with SignalSilence® c-Myc siRNA I #6341, using c-Myc (D84C12) XP® Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using c-Myc (D84C12) XP® Rabbit mAb.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of Raji cells using c-Myc (D84C12) XP® Rabbit mAb (blue) compared to a nonspecific negative control antibody (red).


IF-IC

IF-IC

Confocal immunofluorescent analysis of HeLa cells, mock-transfected (left) or transfected with SignalSilence® c-Myc siRNA I #6341 (right), using c-Myc (D84C12) XP® Rabbit mAb (green). Actin filaments have been labeled wth DY-554 phalloidin (red).

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).

  1. Baudino, T.A. and Cleveland, J.L. (2001) Mol. Cell. Biol. 21, 691-702.
  2. Blackwood, E.M. and Eisenman, R.N. (1991) Science 251, 1211-1217.
  3. Henriksson, M. and Lüscher, B. (1996) Adv. Cancer Res. 68, 109-182.
  4. Grandori, C. et al. (2000) Annu. Rev. Cell Dev. Biol. 16, 653-699.

Application References

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Companion Products

This product is intended for research purposes only. The product is not intended to be used for therapeutic or diagnostic purposes in humans or animals.

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