Polyclonal Anti-MAX

Price

200.00 USD

Size

100ug/vial

Reactivities

Hum, Mouse, Rat

Format

Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3.

References

1. Blackwood, E., Eisenman, R. N. Max: a helix-loop-helix zipper protein that forms a \nsequence-specific DNA-binding complex with Myc.Science 251: 1211-1217, 1991.\n2. Gilladoga, A. D., Edelhoff, S., Blackwood, E. M., Eisenman, R. N., Disteche, C. M. Mapping \nof MAX to human chromosome 14 and mouse chromosome 12 by in situ hybridization. Oncogene 7: \n1249-1251, 1992.\n3. Hopewell, R., Ziff, E. B. The nerve growth factor-responsive PC12 cell line does not express the \nMyc dimerization partner Max. Molec. Cell Biol. 15: 3470-3478, 1995.

Storage Temp

At -20 degree C for one year. After reconstitution, at 4 degree C for one month. It can also be aliquotted and stored frozen at -20 degree C for a longer time.Avoid repeated freezing and thawing.

Scientific Background

MAX(Max protein), also called Myc-associated factor x, is the most conserved dimerization component \nof the MYC-MAX-MXD1 network of basic helix-loop-helix leucine zipper (bHLHZ) transcription factors \nthat regulate cell proliferation, differentiation, and apoptosis. The conservation of the MAX sequence is\nparticularly high in the bHLHZ domain, which is involved in protein-protein interactions and DNA binding.\nThe MAX gene is located on chromosome 14q23 by fluorescence in situ chromosomal hybridization.\nBoth quasisymmetric heterodimers resemble the symmetric MAX homodimer, albeit with marked \nstructural differences in the coiled-coil leucine zipper regions that explain preferential homo- and \nheteromeric dimerization of these 3 evolutionarily related DNA-binding proteins. MAX acts as a classic \ntumor suppressor gene. Normal lymphocytes from patients showed absence of methylation of \nthe MAX promoter and biallelic expression of MAX, which ruled out an imprinting-mediated effect \non MAX expression. The ability of these cells to divide, differentiate, and apoptose in the absence \nof Max demonstrated for the first time that these processes can occur via Max- and possibly \nMyc-independent mechanisms.