Lindemann-type mechanism

In terms of a simple Hinshelwood - Lindemann type mechanism this would be... 

According to the Lindemann-Christiansen hypothesis, formulated independently by both scientists in 1921, all molecules acquire and lose energy by collisions with surrounding molecules. This is expressed in the simplified form of the Lindemann mechanism, in which we use an asterisk to indicate a highly energetic or activated molecule, which has sufficient energy to cross the barrier towards the product side, and M is a molecule from the surroundings M may be from the same type as A ... 

The simplest type of system that obeys equation (17) is the unimolecular process 95li products. Since a stable molecule should not spontaneously break up into reaction products, the mechanism by which the unimolecular process occurs must be explained. Many unimolecular reactions are believed to follow the mechanism proposed by Lindemann, namely. 

If we further take fe = 0 this becomes the Lindemann mechanism that is used to explain the observation that many gas-phase reactions of the type A product that appear unimolecular at high pressure change their character to bimolecular at low pressure. Lindemann has postulated that such unimolecular reactions proceed... 

If one role of PKG is to decrease smooth muscle intracellular Ca levels, then the mechanism by which this occurs is still not completely defined. Several protein substrates that are known to be phosphorylated by activation of PKG have been identified in SMCs, platelets, and other tissues. Interestingly, some of these proteins have been shown by others to regulate intracellular Ca levels in various cell types. For example, phospholamban, when phosphorylated by PKA in cardiac myocytes, dissociates from sarcoplasmic reticulum (SR) Ca -ATPase resulting in the enhanced sequestration of Ca into the SR (Lindemann et al., 1983). A similar effect of PKG activation has been shown in SMCs (Cornwell et al., 1991 Karczewski et al., 1992 Raeymaekers et al., 1988 Sarcevic et al., 1989). Using another example, Supattopone et al. (1988) reported that PKA-dependent phosphorylation of the inositol 1,4,5-trisphosphate (IP3) receptor in broken-cell fractions decreased Ca release from brain microsomes. Our laboratory has recently shown that the IP3 receptor is also phosphorylated by PKG in vitro on the major PKA phosphorylation site (i.e., Ser-1755) (Komalavilas and Lincoln,... 

---