๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Inhibition of T-cell activation by syndecan-4 is mediated by CD148 through protein tyrosine phosphatase activity

โœ Scribed by Jin-Sung Chung; Ponciano D. Cruz Jr.; Kiyoshi Ariizumi


Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
352 KB
Volume
41
Category
Article
ISSN
0014-2980

No coin nor oath required. For personal study only.


๐Ÿ“œ SIMILAR VOLUMES


Signal transduction through cd4 receptor
โœ Jeffrey A. Ledbetter; Carl H. June; Peter S. Rabinovitch; Angelika Grossmann; Th ๐Ÿ“‚ Article ๐Ÿ“… 1988 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 892 KB

## Signal transduction through CD4 receptors: stimulatory vs. inhibitory activity is regulated by CD4 proximity to the CD31T cell receptor* The binding of antibody to the CD4 molecule inhibits mobilization of cytoplasmic free calcium ([Ca2'Ii) in response to CD3 cross-linking on resting T cells. S

B7-H4 mediates inhibition of T cell resp
โœ Raghavan Chinnadurai; Arash Grakoui ๐Ÿ“‚ Article ๐Ÿ“… 2010 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 890 KB

Liver fibrosis is mediated by the transformation of hepatic stellate cells (HSC) from a quiescent to an activated state. To understand the role of HSC in liver immunity, we investigated the effect of this transition on T cell stimulation in vitro. Unlike quiescent HSC, activated HSC did not induce p

Retinoic acid induced repression of AP-1
โœ Carmilia Jimรฉnez Ramรญrez; Juliet M. Haberbusch; Dianne Robert Soprano; Kenneth J ๐Ÿ“‚ Article ๐Ÿ“… 2005 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 278 KB

## Abstract In previous studies we have shown that __all__โ€__trans__ retinoic acid (__at__RA)โ€treatment of the __at__RAโ€sensitive ovarian carcinoma cell line CAโ€OV3 repressed APโ€1 activity by about 50%, while a similar effect was not observed in the __at__RAโ€resistant ovarian carcinoma cell line, S

Activation of protein phosphatase-2A1 by
โœ Anwar Janoo; Peter W. Morrow; H.Y. Lim Tung ๐Ÿ“‚ Article ๐Ÿ“… 2005 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 209 KB

HIV-1, the etiologic agent of human AIDS, causes cell death in host and non-host cells via HIV-1 Vpr, one of its auxiliary gene product. HIV-1 Vpr can also cause cell cycle arrest in several cell types. The cellular processes that link HIV-1 Vpr to the cell death machinery are not well characterized