Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 1998 Sep 7;188(5):931–939. doi: 10.1084/jem.188.5.931

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

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/).

PMC Copyright notice

Possible models for the positioning of Rho in p56lck-mediated signaling pathways regulating various aspects of pre-T cell development. (A) The pre-TCR initiates signaling pathways mediated by p56lck that regulate thymocyte development and control the process of allelic exclusion of the TCR-β locus in pre-T cells. A possible model consistent with our data locates Rho either directly downstream of p56lck or in parallel signaling pathways controlling proliferation and regulation of CD2 expression in pre-T cells. Other signals emerging from p56lck-regulating inhibition of TCR-β chain rearrangement are Rho independent. Dashed arrows symbolize as yet formally unproven links between the pre-TCR, p56lck and Rho. (B) An alternative model compatible with our results depicts Rho as a signal amplifier which increases the signal intensity generated by p56lck. Individual biological responses regulated by the pre-TCR would be dependent on different signal intensities and would only be initiated if the signaling strength generated by p56lck and Rho would reach their individual thresholds. Thus, signal intensity in the absence of Rho function would still be sufficient to mediate inhibition of TCR-β chain rearrangement but not to downregulate CD2 expression or drive pre-T cell proliferation.

Possible models for the positioning of Rho in p56lck-mediated signaling pathways regulating various aspects of pre-T cell development. (A) The pre-TCR initiates signaling pathways mediated by p56lck that regulate thymocyte development and control the process of allelic exclusion of the TCR-β locus in pre-T cells. A possible model consistent with our data locates Rho either directly downstream of p56lck or in parallel signaling pathways controlling proliferation and regulation of CD2 expression in pre-T cells. Other signals emerging from p56lck-regulating inhibition of TCR-β chain rearrangement are Rho independent. Dashed arrows symbolize as yet formally unproven links between the pre-TCR, p56lck and Rho. (B) An alternative model compatible with our results depicts Rho as a signal amplifier which increases the signal intensity generated by p56lck. Individual biological responses regulated by the pre-TCR would be dependent on different signal intensities and would only be initiated if the signaling strength generated by p56lck and Rho would reach their individual thresholds. Thus, signal intensity in the absence of Rho function would still be sufficient to mediate inhibition of TCR-β chain rearrangement but not to downregulate CD2 expression or drive pre-T cell proliferation.