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Results: 3

1.
Figure 3

Figure 3. From: The LIM and SH3 domain protein family: structural proteins or signal transducers or both?.

Model of the putative function of LASP-1 as a zyxin recruiting protein. Upper panel: physiological situation with normal LASP-1 expression. Lower panel: pathological situation in an LASP-1 overexpressing cell and subsequent disruption of zyxin signalling. CD44 and Ezrin are integrated into this figure as possible upstream interaction partners because of their close colocalization to LASP-1 and Krp1, albeit neither direct nor indirect interaction has been proved yet.

Thomas GP Grunewald, et al. Mol Cancer. 2008;7:31-31.
2.
Figure 2

Figure 2. From: The LIM and SH3 domain protein family: structural proteins or signal transducers or both?.

Schematic models of LASP-1 and LASP-2 domain structures. Identified binding partners are indicated at the appropriate domains (Krp1 – Kelch related protein 1, LPP – lipoma preferred partner, VASP – vasodilator stimulated phosphoprotein, Pro-IL-16 – Prointerleukin-16). Known phosphorylation sites at serine 146 (S146) and tyrosine 171(Y171) are marked with pink boxes.

Thomas GP Grunewald, et al. Mol Cancer. 2008;7:31-31.
3.
Figure 1

Figure 1. From: The LIM and SH3 domain protein family: structural proteins or signal transducers or both?.

Relative expression pattern of murine (black columns) and human (gray columns) LASP-1 of selected tissues in part adapted from Su et al. 2002 [22]. The median of LASP-1 expression in all tissue types that have been originally analyzed by Su et al. was set at 100% (blue line); two fold value of the median is indicated in red. As seen in the graph LASP-1 is expressed in a wide variety of human and murine tissues. High to excessive expression is observed during early embryonic development, in immunocompetent cells, fetal brains, muscle cells, entire blood and colorectal carcinomas. Interestingly, LASP-1 is not expressed at high levels in benign tissues of the reproductive tract (ovary and mammary gland), but has been reported to be overexpressed in metastases of malign tumours derived from these tissues.

Thomas GP Grunewald, et al. Mol Cancer. 2008;7:31-31.

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