|Application ||WB, IP|
|Calculated MW||83067 Da|
|Application & Usage||Western blotting (1:500 – 1:2000) and Immunoprecipitation. HeLa cell lysate can be used as a positive control. However, the optimal concentrations should be determined individually. The antibody recognizes the MAD1 of human and mouse origins. Reactivity to other species has not been tested.|
|Other Names||MAD1, MAD-1, MADL1, HsMAD1, Mitotic arrest deficient-like 1, PIG9, p53 inducible protein 9, TP53I9, tumor protein p53 inducible protein 9, TXBP181, Tax binding protein-181|
|Formulation||100 µl affinity purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 30% glycerol, 1% BSA and 0.02% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||MAD1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Component of the spindle-assembly checkpoint that prevents the onset of anaphase until all chromosomes are properly aligned at the metaphase plate. May recruit MAD2L1 to unattached kinetochores. Has a role in the correct positioning of the septum. Required for anchoring MAD2L1 to the nuclear periphery. Binds to the TERT promoter and represses telomerase expression, possibly by interfering with MYC binding.|
|Cellular Location||Nucleus. Chromosome, centromere, kinetochore. Nucleus envelope. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Cytoplasm, cytoskeleton, spindle. Cytoplasm, cytoskeleton, spindle pole. Note=Detected at the nucleus envelope during interphase (PubMed:22351768). From the beginning to the end of mitosis, it is seen to move from a diffusely nuclear distribution to the centrosome, to the spindle midzone and finally to the midbody. Detected at kinetochores during prometaphase (PubMed:22351768). Colocalizes with NEK2 at the kinetochore (PubMed:14978040). Colocalizes with IK at spindle poles during metaphase and anaphase (PubMed:22351768)|
|Tissue Location||Expressed weakly at G0/G1 and highly at late S and G2/M phase|
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Provided below are standard protocols that you may find useful for product applications.
Cell cycle progression is subject to arrest at the mitotic spindle assembly checkpoint in response to incorrect spindle fiber assembly. MAD1 and MAD2 (for mitotic arrest-deficient 1 and 2) are components of the mitotic spindle checkpoint. Incorrect spindle assembly in normal cells leads to mitotic arrest. MAD1 prevents the onset of anaphase until all chromosomes are aligned correctly at the metaphase plate and is crucial for anchoring MAD2L1 to the nuclear periphery. It also plays an important role in septum positioning. MAD1 can form a homo-dimer, but may also form a heterodimer with MAD2 to form the tetrameric MAD1L1-MAD2L1 core complex. MAD1 localizes primarily to the nucleus, but during mitosis, it moves from a nuclear distribution to the centrosome, to the spindle midzone and then on to the midbody. MAD1 activity is induced by BUB1 and the protein is hyperphosphorylated after mitotic spindle damage and/or in late S through M phase. Defects in the gene encoding for MAD1, MAD1L1, play a major role in the development and progression of various cancer types.
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