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. 1999 Jul 1;190(1):101–112. doi: 10.1084/jem.190.1.101

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© 1999 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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The effects of mutant TCS on chemokine receptor activation and chemotaxis. THP-1 cells were stimulated with SDF-1α (10 nM) in the absence or presence of TCS (isolated from T. kirilowii), r-TCS (recombinant TCS expressed in E. coli), or m-TCS (mutation at position 120–123) (0.2 μM for [³⁵S]GTPγS binding and 2 nM for chemotaxis). [³⁵S]GTPγS binding (A) and chemotaxis (B) were determined as described in Materials and Methods. Data were mean ± SE of at least two independent experiments performed in duplicate. The purities of TCS, r-TCS, and m-TCS were examined using silver staining after SDS-PAGE (C).

The effects of mutant TCS on chemokine receptor activation and chemotaxis. THP-1 cells were stimulated with SDF-1α (10 nM) in the absence or presence of TCS (isolated from T. kirilowii), r-TCS (recombinant TCS expressed in E. coli), or m-TCS (mutation at position 120–123) (0.2 μM for [³⁵S]GTPγS binding and 2 nM for chemotaxis). [³⁵S]GTPγS binding (A) and chemotaxis (B) were determined as described in Materials and Methods. Data were mean ± SE of at least two independent experiments performed in duplicate. The purities of TCS, r-TCS, and m-TCS were examined using silver staining after SDS-PAGE (C).