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The Journal of Neuroscience, March 1, 2006, 26(9):2403-2412; doi:10.1523/JNEUROSCI.4691-05.2006

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Cellular/Molecular
TRPV1 Recapitulates Native Capsaicin Receptor in Sensory Neurons in Association with Fas-Associated Factor 1

Sangsung Kim,^1 * Changjoong Kang,^2 * Chan Young Shin,³ Sun Wook Hwang,⁴ Young Duk Yang,¹ Won Sik Shim,¹ Min-Young Park,⁵ Eunhee Kim,⁵ Misook Kim,¹ Byung-Moon Kim,¹ Hawon Cho,¹ Youngki Shin,¹ and Uhtaek Oh¹

¹Sensory Research Center, College of Pharmacy, Seoul National University, Seoul 151-742, Korea, ²College of Life Science, Kyunghee University, Suwon 449-701, Korea, ³Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut 06520-8103, ⁴Graduate School, College of Medicine, Korea University, Ansan 425-707, Korea, and ⁵Division of Chemistry and Biochemistry, Chungnam National University, Daejeon 305-764, Korea

Correspondence should be addressed to Dr. Uhtaek Oh, College of Pharmacy, Seoul National University, Kwanak, Shinlim 9-dong, Seoul 151-742, Korea. Email: utoh{at}plaza.snu.ac.kr

TRPV1, a cloned capsaicin receptor, is a molecular sensor for detecting adverse stimuli and a key element for inflammatory nociception and represents biophysical properties of native channel. However, there seems to be a marked difference between TRPV1 and native capsaicin receptors in the pharmacological response profiles to vanilloids or acid. One plausible explanation for this overt discrepancy is the presence of regulatory proteins associated with TRPV1. Here, we identify Fas-associated factor 1 (FAF1) as a regulatory factor, which is coexpressed with and binds to TRPV1 in sensory neurons. When expressed heterologously, FAF1 reduces the responses of TRPV1 to capsaicin, acid, and heat, to the pharmacological level of native capsaicin receptor in sensory neurons. Furthermore, silencing FAF1 by RNA interference augments capsaicin-sensitive current in native sensory neurons. We therefore conclude that FAF1 forms an integral component of the vanilloid receptor complex and that it constitutively modulates the sensitivity of TRPV1 to various noxious stimuli in sensory neurons.

Key words: TRPV1; FAF1; association; pharmacology; capsaicin; pain

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Received Nov. 2, 2005; revised Jan. 2, 2006; accepted Jan. 9, 2006.

Correspondence should be addressed to Dr. Uhtaek Oh, College of Pharmacy, Seoul National University, Kwanak, Shinlim 9-dong, Seoul 151-742, Korea. Email: utoh{at}plaza.snu.ac.kr

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