Hyaluronidases regulation

Maksimenko, A. V, Petrova, M. L., Tischenko, E. G., and Schechilina, Y. V. (2001). Chemical modification of hyaluronidase regulates its inhibition by heparin. European Journal of Pharmaceutics and Biopharmaceutics 51, 33-38. 

A vertebrate homologue of the cell cycle control protein CDC37 was recently cloned and found to be an hyaladherin,62 as was a protein that copurified with the splicing factor SF2.63 An intracellular form of the HA receptor RHAMM was demonstrated to regulate erk kinase activity. Changes in function of these intracellular, depending on whether or not they have HA molecules attached, confers another layer of complexity dependent on intracellular hyaluronidase enzymes. 

Junker, N. et al., Expression and regulation patterns of hyaluronidases in small cell lung cancer and glioma lines, Oncol. Rep., 10, 609, 2003. 

Pogrel, M., Low, M., and Stem, R. (2003) Hyaluronan (hyaluronic acid) and its regulation in human saliva by hyaluronidase and its inhibitors. Journal of Oral Science, 45, 85-91. 

In humans, contact with LPS may occur not only during a bacterial infection but also via LPS-contaminated medicaments and solutions administrated intravenously (parenteralia). Since the biological effects of LPS may appear even at concentrations of 1 ng per 1 kg of body weight, drugs intended for parenteral use, have to be endotoxin-free , i.e., thoroughly depyrogenated. In fact parenteralia have to comply with LPS threshold limits (in EU , endotoxin unit) regulated by pharmacopoeias. For example, tetracycline hydrochloride may not contain more than 0.5 ELf/mg. Similar limits exist for insulin (0.8 EU/insulin unit), hyaluronidase (2.3 EU/ hyaluronidase unit), the sodium salt ofheparin for injection (0.003 EU/heparin unit). ... 

---