3-Azioctanol Photolabels A Site On The Neural Cell Adhesion Molecule, L1

Arevalo, E; Wilkemeyer, MF; Shanmugasundararaj, S; Charness, ME; Miller, KW

HERO ID

1455492

Reference Type

Journal Article

Year

2006

Language

eng

HERO ID 1455492
In Press No
Year 2006
Title 3-Azioctanol Photolabels A Site On The Neural Cell Adhesion Molecule, L1
Authors Arevalo, E; Wilkemeyer, MF; Shanmugasundararaj, S; Charness, ME; Miller, KW
Journal Alcoholism: Clinical and Experimental Research
Volume 30
Issue 6 Suppl
Page Numbers 118A-118A
Abstract Prenatal ethanol exposure results in a spectrum of birth defects and neurobehavioral abnormalities referred to as fetal alcohol spectrum disorders (FASD). One potentially important ethanol target is the L1 neural cell adhesion molecule. L1 is a transmembrane glycoprotein composed of six Ig domains and five fibronectin-type III domains, followed by transmembrane and intracellular domains. Short-chain alcohols (e.g., ethanol and butanol derivatives) show remarkable structural specificity for inhibition of L1-mediated cell adhesion. Other alcohols (e.g., 1-octanol) antagonize ethanol inhibition of L1 cell adhesion and ethanol teratogenesis in mouse whole embryo cultures. To test the hypothesis that there are antagonist binding sites on L1, we have employed the photoactivatable analog of octanol, 3-azioctanol. This agent is remarkably potent at antagonizing ethanol inhibition of L1 adhesion. Azioctanol photoincorporated into a soluble model of L1, consisting of only the six Ig domains. After photolabeling, this polypeptide was digested with trypsin and analyzed by mass spectrometry, which identified Tyr-417 (Y417) and Glu-33 (E33) as sites of photoincorporation. Preliminary modeling of L1, based on the known structure of the homologous 1 and #150;4 Ig domains of axonin-1, suggests that E33 and Y417, on Ig1 and Ig4 respectively, may reside in a single pocket formed by the two Ig domains. Furthermore L120 and G121, in which mutations in humans are associated with neurological disorders, are adjacent to this pocket. Thus, this site likely has functional significance. Identification of the antagonist site will aid in understanding the molecular basis for FASD and may accelerate the development of drugs that block the toxic effects of ethanol on the developing nervous system.
Is Certified Translation No
Dupe Override No
Conference Name 29th Annual Meeting of the Research-Society-on-Alcoholism
Conference Date JUN 23-29, 2006
Is Public Yes
Language Text eng