Polyclonal Anti-BCL2L3

Price

200.00 USD

Size

100ug/vial

Reactivities

Hum

Format

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

References

1. Inuzuka, H., Shaik, S., Onoyama, I., Gao, D., Tseng, A., Maser, R. S., Zhai, B., Wan, L., Gutierrez, A., Lau, A. W., Xiao, Y., Christie, A. L., Aster, J., Settleman, J., Gygi, S. P., Kung, A. L., Look, T., Nakayama, K. I., DePinho, R. A., Wei, W.SCF(FBW7) regulates cellular apoptosis by targeting MCL1 for ubiquitylation and destruction.Nature 471: 104-109, 2011.\n2. Leu, J. I.-J., Dumont, P., Hafey, M., Murphy, M. E., George, D. L.Mitochondrial p53 activates Bak and causes disruption of a Bak-Mcl1 complex.Nature Cell Biol. 6: 443-450, 2004.\n3. Schwickart, M., Huang, X., Lill, J. R., Liu, J., Ferrando, R., French, D. M., Maecker, H., O'Rourke, K., Bazan, F., Eastham-Anderson, J., Yue, P., Dornan, D., Huang, D. C. S., Dixit, V. M.Deubiquitinase USP9X stabilizes MCL1 and promotes tumour cell survival.Nature 463: 103-107, 2010.\n

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.\nAvoid repeated freezing and thawing. \n\"\n

Scientific Background

BCL2L3, also known as MCL1(myeloid cell leukemia sequence 1) encodes an anti-apoptotic protein, which is a member of the Bcl-2 family. Alternative splicing results in multiple transcript variants. The longest gene product (isoform 1) enhances cell survival by inhibiting apoptosis while the alternatively spliced shorter gene products (isoform 2 and isoform 3) promote apoptosis and are death-inducing.Using the methods of somatic cell hybrid analysis and fluorescence in situ hybridization), the MCL1 gene is mapped to human 1q21.MCL1is a critical and specific regulator essential for ensuring the homeostasis of early hematopoietic progenitors.Phosphorylation of MCL1 directs its interaction with the tumor suppressor protein FBW7, which is the substrate-binding component of a ubiquitin ligase complex. The polyubiquitylation of MCL1 then targets it for proteasomal degradation. The degradation of MCL1 was blocked in patient-derived tumor cells that lacked FBW7 or had loss-of-function mutations in FBW7, conferring resistance to antitubulin agents and promoting chemotherapeutic-induced polyploidy.