上海研卉生物支原體預防與清除利器，PlasmocinTM prophylactic優惠促銷

支原體預防與清除利器，支原體清除，支原體預防，Mycoplasma Removal Agent
產品優勢：1，預防支原體、細菌、真菌污染
2，只需2周即可清除支原體污染
3，不會影響細胞本身代謝
4， 不會重新感染（從其他細胞釋放的）支原體

Plasmocin?

Mycoplasma Removal Agent

Plasmocin? is used to

and related cell wall-less bacteria.

Plasmocin? can also be used as a routine addition in liquid media toprevent mycoplasma and more generally bacterial contamination in smalland large animal cell cultures.

Plasmocin? is a well-established antimycoplasma reagent. It contains two bactericidal components strongly active against mycoplasmas that allow their elimination in only 2 weeks.
The first component acts on the protein synthesis machinery while the second acts on the DNA replication. These two specific and separate targets are found only in mycoplasmas and many other bacteria and are completely absent in eukaryotic cells.

Warning: InvivoGen's anti-mycoplasma products are suitable for research purposes only, and not for human or animal care.

Plasmocin? prophylactic
2.5 mg/ml (Plasmocin? Prophylactic)

Plasmocin? treatment

Comparison of the most common anti-mycoplasma agents[1-3]

對照表

Antibiotics commonly used in cell culture are inactive on mycoplasma (e.g. penicillins and streptomycin). Three classes of antibiotics have been shown to kill mycoplasma at relatively low concentrations: tetracyclines, macrolides and quinolones. Tetracyclines and macrolides block the protein synthesis by interfering with ribosome translation, while quinolones inhibit the replication of bacterial DNA.
Several antibiotics are commercially available for the removal of mycoplasma: BM-cyclin (Roche) contains a macrolide and a tetracycline, Ciprobay (Bayer, available only with a prescription) and MRA (ICN) are both quinolones. Plasmocin? is the only antimycoplasma reagent that combines a macrolide and a quinolone. Unlike BM-Cyclin that requires the sequential and cyclic use of 2 antibiotics, Plasmocin? is ready-to-use and can be added to the culture medium directly. Furthermore, the 2 antibiotics in Plasmocin? act on separate targets blocking protein synthesis and DNA replication, whereas the 2 antibiotics in BM-Cyclin are both inhibitors of protein synthesis. Therefore, Plasmocin? is more effective in removing mycoplasma and prevents the appearance of resistant strains. In contrast to other anti-mycoplasma compounds, Plasmocin? is active on both free mycoplasma as well as intracellular forms. This advantage is conferred by one component of Plasmocin? which is actively transported into mammalian cells. It ensures that following treatment with Plasmocin? a cell culture is not reinfected by mycoplasma released from intracellular compartments of infected cells. To date, no consistent and permanent alterations that affect the eukaryotic cells during and after the treatment have been detected[1].

1. Uphoff CC, Drexler HG., 2005. Eradication of mycoplasma contaminations. Methods Mol Biol. 290:25-34.
2. Somasundaram C. et al., 1992. Use of ciprofloxacin and BM-Cyclin in mycoplasma decontamination.In Vitro Cell Dev Biol. 28A(11-12):708-10
3. Drexler HG. et al., 1994. Treatment of mycoplasma contamination in a large panel of cell cultures. In vitro Cell Dev Biol Anim. 30A(5):344-7

參考文獻：

Recent articles using Plasmocin?

• 2012 - J Virol Methods., 187(2):234-7
  Mycoplasma removal: Simple curative methods for viral supernatants.
  Baronti C, Pastorino B, Charrel R, de Lamballerie X
• 2011 - Mol Pharmacol., 80(6):1066-75
  Ca2+/calmodulin-dependent kinase (CaMK) signaling via CaMKI and AMP-activated protein kinase contributes to the regulation of WIPI-1 at the onset of autophagy.
  Pfisterer SG, Mauthe M, Codogno P, Proikas-Cezanne T
• 2011 - J Immunol., 186(12):6822-6829
  Tumor cell programmed death ligand 1-mediated T cell suppression is overcome by coexpression of CD80.
  Haile ST, Bosch JJ, Agu NI, Zeender AM, Somasundaram P, Srivastava MK, Britting S, Wolf JB, Ksander BR, Ostrand-Rosenberg S
• 2012 - J. Biol. Chem., 287: 8082 - 8091
  Loss of lysosomal ion channel transient receptor potential channel mucolipin-1 (TRPML1) leads to cathepsin B-dependent apoptosis.
  Colletti GA, Miedel MT, Quinn J, Andharia N, Weisz OA, Kiselyov K
• 2012 - Immunity, 36(3):464-476
  An NLRP7-containing inflammasome mediates recognition of microbial lipopeptides in human macrophages.
  Khare S, Dorfleutner A, Bryan NB, Yun C, Radian AD, de Almeida L, Rojanasakul Y, Stehlik C