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These data suggest that prolactin receptors are retained intracellularly because of their incomplete N-glycosylation and that NO triggers their redistribution by stimulating the completion of this process, in part by increasing NAG transferase I activity.
Our observations suggest that prolactin induces its own receptor.
As little as 0.5 mg prolactin significantly increases receptors, while doses above the 2 mg optimum are apparently less effective.
Open accessJournal ArticleDOI
S. Sakai, M Katoh, P Berthon, P A Kelly 
38 Citations
The present demonstration shows that particulate prolactin receptors from a domestic animal can be solubilized and purified without losing the original properties of high affinity and binding specificity for hormones.
In this report we demonstrate that prolactin regulates the level of cryptic receptors.
Prolactin-receptor-deficient mice are a good model in which to study the various actions of prolactin.
It is now clear that cellular responsiveness to prolactin can be regulated through differential promoter control of the expression of the surface receptors for prolactin in different target tissues.
We now show both recombinant and natural pituitary-derived mouse prolactin to be a poor agonist for human prolactin receptors.
Thus, our results lead to improved understanding of the prolactin-prolactin receptor interaction.
Therefore, it appears that receptors with lower affinity at the cell periphery are those involved in the initial mechanism of action of prolactin.

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