Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

Myt1 Antibody #4282

Applications Reactivity Sensitivity MW (kDa) Source
W IHC-P H M R (X) Endogenous 60 to 70 Rabbit

Applications Key:  W=Western Blotting  IHC-P=Immunohistochemistry (Paraffin)
Reactivity Key:  H=Human  M=Mouse  R=Rat  X=Xenopus
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Myt1 Antibody detects endogenous levels of total Myt1 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the middle of mouse and human Myt1. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from HT29 cells, untreated (lane 1), nocodazole-treated (50 ng/ml, lane 2), or UV-treated (lane 3), using Myt1 Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast carcinoma, showing nuclear and cytoplasmic localization using Myt1 Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human colon carcinoma, using Myt1 Antibody.


IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lung carcinoma, using Myt1 Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human colon carcinoma, using Myt1 Antibody in the presence of control peptide (left) or antigen specific peptide (right).

Background

Entry of all eukaryotic cells into mitosis is regulated by activation of cdc2 kinase. The critical regulatory step in activating cdc2 during progression into mitosis appears to be dephosphorylation of Tyr15 and Thr14 (1,2). Phosphorylation at Tyr15 and Thr14 and inhibition of cdc2 is carried out by Wee1 and Myt1 protein kinases, while Tyr15 dephosphorylation and activation of cdc2 is carried out by the cdc25 phosphatase (1,3,4). Hyperphosphorylation and inactivation of Myt1 in mitosis suggests that one or more kinases activated at the G2/M transition negatively regulates Myt1 activity. Kinases shown to phosphorylate Myt1 include cdc2, p90RSK, Akt, and Plk1 (5-8).

  1. Watanabe, N. et al. (1995) EMBO J. 14, 1878-1891.
  2. Hunter, T. (1995) Cell 80, 225-236.
  3. Galaktionov, K. et al. (1995) Genes Dev. 9, 1046-1058.
  4. McGowan, C.H. and Russell, P. (1993) EMBO J. 12, 75-85.
  5. Booher, R. N. et al. (1997) J. Biol. Chem. 272, 22300-22306.
  6. Palmer, A. et al. (1998) EMBO J. 17, 5037-5047.
  7. Okumura, E. et al. (2002) Nat. Cell Biol. 4, 111-116.
  8. Nakajima, H. et al. (2003) J. Biol. Chem. 278, 25277-25280.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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