TY - JOUR
T1 - Inhibition of contact sensitivity by farnesylthiosalicylic acid-amide, a potential rap1 inhibitor
AU - Mor, Adam
AU - Haklai, Roni
AU - Ben-Moshe, Ofer
AU - Mekori, Yoseph A.
AU - Kloog, Yoel
N1 - Funding Information:
This research was supported by the Morasha Program of the Israel Science Foundation (grant no. 1822/07). Adam Mor has received grant support from the Israel Science Foundation. This work was supported in part by a grant from the Israel Science Foundation to Yoseph Mekori, who is the incumbent of the Reiss Chair in Dermatology, Tel Aviv University. Yoel Kloog is the incumbent of the Skirball Chair in Applied Neurobiology, Tel Aviv University, and is supported by the Prajs-Drimmer Institute for Anti-degenerative Disease Drugs. We would like to thank Luis Chiriboga, PhD, for slide preparation. We would like to acknowledge Dr Mark Philips (NYU) for excellent and substantial scientific and technical support.
PY - 2011/10
Y1 - 2011/10
N2 - We hypothesized that Ras proximate 1 (Rap1) functions as an additional target for farnesylthiosalicylic acid (FTS) or its derivatives, and that the inhibition of Rap1 in lymphocytes by these agents may represent a method for treating inflammatory disorders. Indeed, we found that FTS-amide (FTS-A) was able to inhibit the elicitation phase of delayed cutaneous hypersensitivity in vivo. This effect was associated with the inhibition of Rap1 more than with the inhibition of Harvey rat sarcoma viral oncogene (Ras). Moreover, FTS-A inhibited Rap1 and contact sensitivity far better than FTS. We suggest that FTS-A may serve as a possible therapeutic tool in contact sensitivity in particular and T-cell-mediated inflammation in general.
AB - We hypothesized that Ras proximate 1 (Rap1) functions as an additional target for farnesylthiosalicylic acid (FTS) or its derivatives, and that the inhibition of Rap1 in lymphocytes by these agents may represent a method for treating inflammatory disorders. Indeed, we found that FTS-amide (FTS-A) was able to inhibit the elicitation phase of delayed cutaneous hypersensitivity in vivo. This effect was associated with the inhibition of Rap1 more than with the inhibition of Harvey rat sarcoma viral oncogene (Ras). Moreover, FTS-A inhibited Rap1 and contact sensitivity far better than FTS. We suggest that FTS-A may serve as a possible therapeutic tool in contact sensitivity in particular and T-cell-mediated inflammation in general.
UR - http://www.scopus.com/inward/record.url?scp=80052837784&partnerID=8YFLogxK
U2 - 10.1038/jid.2011.152
DO - 10.1038/jid.2011.152
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C2 - 21716322
AN - SCOPUS:80052837784
SN - 0022-202X
VL - 131
SP - 2040
EP - 2048
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 10
ER -