𝔖 Bobbio Scriptorium
✦   LIBER   ✦

HIV induces activation of phosphatidylinositol 4-kinase and mitogen-activated protein kinase by interacting with T cell CD4 surface molecules

✍ Scribed by Heidy Schmid-Antomarchi; Monsef Benkirane; Violette Breittmayer; Hervé Husson; Michel Ticchioni; Christian Devaux; Bernard Rossi

Publisher
John Wiley and Sons
Year
1996
Tongue
English
Weight
426 KB
Volume
26
Category
Article
ISSN
0014-2980

No coin nor oath required. For personal study only.

✦ Synopsis

HIV induces activation of phosphatidylinositol 4-kinase and mitogen-activated protein kinase by interacting with T cell CD4 surface molecules

T cell surface CD4 molecules act as co-receptors that amplify the T cell receptor (TcR)/CD3-induced signal transduction by a mechanism that requires the interaction of CD4 with ~5 6 ' ' ~ tyrosine kinase (Veillette et al.; Nature 1989.338: 257). Here, we demonstrate that in the absence of TcR signaling, heat-inactivated HIV-1 (HIV-HI) also elicits a cascade of events generally considered to convey a positive signal, such as protein tyrosine phosphorylation, phosphatidylinositol 4-kinase and mitogen-activated protein kinase activation. These results contribute to understand better the control that HIV may exert on its own replication or on T cell apoptosis by modulating the activation status of its target cells through its interaction with T cell surface CD4 molecules.

📜 SIMILAR VOLUMES

Costimulation by CD137/4–1BB inhibits T
Costimulation by CD137/4–1BB inhibits T cell apoptosis and induces Bcl-xL and c-FLIPshort via phosphatidylinositol 3-kinase and AKT/protein kinase B
✍ Lilian Stärck; Christian Scholz; Bernd Dörken; Peter T. Daniel 📂 Article 📅 2005 🏛 John Wiley and Sons 🌐 English ⚖ 333 KB

## Abstract Costimulation is essential for induction of T lymphocyte proliferation and inhibition of activation‐induced cell death. While signaling pathways activated following the ligation of the costimulatory molecule CD28 are well defined, less is known about the molecular events induced by alte

Contributions of mitogen-activated prote
Contributions of mitogen-activated protein kinase and nuclear factor kappa B to N-(4-hydroxyphenyl)retinamide–induced apoptosis in prostate cancer cells
✍ Keiji Shimada; Mitsutoshi Nakamura; Eiwa Ishida; Munehiro Kishi; Shin Yonehara; 📂 Article 📅 2002 🏛 John Wiley and Sons 🌐 English ⚖ 419 KB

## Abstract The synthetic retinoid __N__‐(4‐hydroxyphenyl)retinamide (4‐HPR) has been shown to induce apoptosis in various types of tumors, including prostate cancer. We sought to examine the key mechanisms affecting the resistance to 4‐HPR–induced apoptosis in three human prostate cancer cell line

[8-(Diethylamino)octyl-3,4,5-trimethoxyb
[8-(Diethylamino)octyl-3,4,5-trimethoxybenzoate, HCl], the inhibitor of intracellular calcium mobilization, blocked mitogen-induced T cell proliferation by interfering with the sustained phase of protein Kinase C activation
✍ Sanjeev Kumar; Rabindranath Chakrabarti 📂 Article 📅 2000 🏛 John Wiley and Sons 🌐 English ⚖ 177 KB 👁 1 views

The physiological role of IP 3 -dependent Ca 2ϩ release in T cell activation was in question due to the contradictory findings that [8-(Diethylamino)octyl-3,4,5-trimethoxybenzoate, HCl] (TMB-8), an inhibitor of intracellular Ca 2ϩ mobilization, blocked T cell proliferation, curtailing specifically t