By M Conn, C Kordon & Y Christen (Eds.)
This booklet describes the present kingdom of data in receptor functionality within the improvement of recent medications. technology is at the verge of viewing effector molecules and different regulatory websites as healing ambitions for the amelioration of human and animal ailment. The booklet studies the supply of state of the art instruments that permit size of interactions and have enough money remarkable perception into the biomolecular interactions that current novel ways to drug layout.
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Additional resources for Insights into Receptor Function and New Drug Development Targets (Research and Perspectives in Endocrine Interactions)
M. Conn Functional Rescue of Misfolded Receptor Mutants 31 necessarily non-speciﬁc so that the folded state of each protein can be determined. Generally, recognition of exposed hydrophobic surfaces on proteins signals that a protein is misfolded and will be targeted for re-folding or degradation (Sitia and Braakman 2003). Molecular chaperones such as calnexin/calreticulin and many of the heat shock protein family act as the endoplasmic reticulum folding sensors and direct misfolded proteins to re-folding pathways, to their functional site in the cell or to degradation pathways (Schroder and Kaufman 2005).
This last etiology was identiﬁed in patients who were diagnosed with HH but were unresponsive to treatment with exogenous GnRH analogs (de Roux et al. 1997). P. M. Conn Further identiﬁcation of such GnRH-resistant HH patients and subsequent sequencing of their GnRH receptor revealed that mutations were compound heterozygous and led to partially or completely inactive receptor proteins. To date, there have been 18 different mutations of the GnRHR gene isolated from GnRH-resistant HH patients. One mutation causes incorrect mRNA splicing, resulting in mis-insertion of a stop codon and a resultant 177 residue peptide (compared to the 328 residue full length protein; Silveira et al.
In anterior pituitary, the presence of proconvertase 1 (PC1) enzyme allows the production of ACTH and β- lipotropin peptides whereas the presence of both PC1 and PC2 in hypothalamus determines the production of α-, β-, γ-MSH and β-endorphins. A recent and elegant work using a Cre/loc strategy that creates mice with POMC neuron degeneration showed that POMC-ablation mice develop obesity but with a defect in compensatory hyperphagia, in contrast to the phenotype of POMC-KO mice (Xu et al. 2005). This work clearly emphasizes the role of POMC neurons in controlling adiposity.
Insights into Receptor Function and New Drug Development Targets (Research and Perspectives in Endocrine Interactions) by M Conn, C Kordon & Y Christen (Eds.)