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These differences might explain the functional differences observed between putrescine and spermine.
2
The threshold for activation by spermine was approximately 500 microm at room temperature.
3
A novel antagonist to that receptor nullified the attraction of ovulatory females to spermine.
4
Spermidine had a weaker effect than spermine whereas putrescine had no effect on insulin binding.
5
The extent of phosphorylation was no longer increased by spermine or EGF, but was inhibited by heparin.
6
This suggests another role of spermine in the MMTS generation in addition to the induction of apoptosis.
7
We determined that spermine, an odorous polyamine initially identified from human semen, is indeed a milt pheromone.
8
Competition curves with unlabelled insulin indicated that spermine increased the insulin binding capacity without significantly affecting the binding affinity.
9
This process was delayed by a-difluoromethylornithine, but spermine increased the latency and time of reversal and decreased receptor desensitization.
10
Measurement of polyamine levels revealed a marked decrease in spermine in liver and pancreas of affected male Gy mice.
11
On the contrary, spermine or SB202190 attenuated the reduction of infarct size and lactate dehydrogenase release induced by remote preconditioning.
12
Uptake of the fluoroquinolone was decreased in both cases; the initial rate of penetration decreased as more spermine blocked the channel.
13
This is achieved by bending the major groove of DNA over spermine and altering oligomer sugar puckering and interstrand phosphate distances.
14
Following the exfoliation, the cell growth restarted from the fresh periphery of EB in a spermine-free medium and finally formed MMTS.
15
During spermine treatment for 24 h, a monolayer cell sheet that had already grown radially from the periphery of an EB was exfoliated.
16
In particular a large spermine catabolism is induced by RA, while DFMO treatment leads to a small increase in the level of this compound.