Viewpoints:

Dispatches from the Frontlines of Research - edited by John W. Nelson

Wenqing Gao and James T. Dalton

Ockham’s Razor and Selective Androgen Receptor Modulators (SARMs): Are We Overlooking the Role of 5-Reductase?
Mol. Interv. 2007 7: 10-13. [Summary] [Full Text] [PDF]  

Mark Nichols

The Fight Against Tamoxifen Resistance in Breast Cancer Therapy: A New Target in the Battle?
Mol. Interv. 2007 7: 13-16. [Summary] [Full Text] [PDF]  

R E V I E W S:

Holger Römpler, Claudia Stäubert, Doreen Thor, Angela Schulz, Michael Hofreiter, and Torsten Schöneberg

G Protein-Coupled Time Travel: Evolutionary Aspects of GPCR Research
Mol. Interv. 2007 7: 17-25. [Summary] [Full Text] [PDF]  

The common seven-transmembrane–domain (TMD) architecture of G protein–coupled receptors (GPCRs) has been preserved over a vast period of time, and highly conserved amino acid motifs and residues have evolved to establish ligand and signal transduction specificities. Because the structure of only a single GPCR has been successfully described at high resolution (i.e., bovine rhodopsin), sequence comparisons among species have been sought as an alternative source of structure–function information about GPCRs. The mining of evolutionary data from sequenced genomes and targeted retrieved orthologs has proven helpful for understanding the physiological relevance of individual GPCRs and for interpreting the clinical significance of GPCR mutations in structural terms. Sequence analysis of GPCR pseudogenes, which are considered as genomic traces of past functions, as well as recent success in sequence analysis of GPCR genes from extinct species, provide further information. This review discusses recent advances and approaches aimed at developing a better understanding of GPCR biology based on evolutionary data.

Grant D. Nicol and Michael R. Vasko

Unraveling the Story of NGF-mediated Sensitization of Nociceptive Sensory Neurons: ON or OFF the Trks?
Mol. Interv. 2007 7: 26-41. [Summary] [Full Text] [PDF] [Erratum]   

Nerve growth factor (NGF) is a well-studied neurotrophin, which by definition is necessary in development for the differentiation of neurons and the proper functioning of nervous tissues. In the adult, however, NGF appears to function primarily to mediate inflammatory and immune responses after tissue injury, especially to initiate and maintain hypersensitivity, a hallmark symptom of inflammation. As part of the inflammatory response, NGF directly or indirectly alters the sensitivity of small diameter sensory neurons that communicate noxious information. The receptors and intracellular signaling cascades that mediate this sensitizing action of NGF are not yet fully elaborated. Although the general consensus is that NGF produces peripheral sensitization by activating the neurotrophin receptor (NTR) TrkA, recent work suggests that the p75 NTR also contributes. The extent to which the two NTRs act independently or together remains to be determined. Furthermore, controversy exists as to the downstream signaling pathways involved in NGF-induced peripheral sensitization.

D E P A R T M E N T S:

Reflections:

Science in the cultural context

Stanley Scheindlin

CLINICAL ENZYMOLOGY: Enzymes As Medicine
Mol. Interv. 2007 7: 4-8. [Full Text] [PDF]  

Nascent Transcripts:

Emerging concepts from the recent literature
Mol. Interv. 2007 7: 9. [Full Text] [PDF]  

Beyond the Bench:

Representations of pharmacology and science in the media

Dayle Houston

"Know Thyself"
Mol. Interv. 2007 7: 42-43. [Full Text] [PDF]  

Net Results:

Sites of interest on the World Wide Web

Sites of interest on the World Wide Web—edited by David Roman
Mol. Interv. 2007 7: 44. [Full Text] [PDF]  

Outliers:

Cartoon

Outliers
Mol. Interv. 2007 7: 52. [Full Text] [PDF]  

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