

Supplier:
Boster ImmunoleaderCat no: PA1768
Polyclonal Anti-MAX
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SPECIFICATIONS
Price
200.00 USD
Catalog Number
PA1768
Size
100ug/vial
Applications
WB
Reactivities
Hum, Mouse, Rat
Form
Lyophilized
Format
Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3.
Gene Id
MAX
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.
Swiss Prot
P61244
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.
Additional Info
A synthetic peptide corresponding to a sequence at the N-terminal of \nhuman MAX, identical to the related rat and mouse sequences .
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.
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