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AKTivation of PI3K/AKT/mTOR signaling pathway by KSHV.

Bhatt AP, Damania B - Front Immunol (2013)

Bottom Line: As an obligate intracellular parasite, Kaposi sarcoma-associated herpesvirus (KSHV) relies on the host cell machinery to meet its needs for survival, viral replication, production, and dissemination of progeny virions.KSHV is a gammaherpesvirus that is associated with three different malignancies: Kaposi sarcoma (KS), and two B cell lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman's disease.We review the mechanisms by which KSHV manipulates the PI3K/AKT/mTOR pathway, with a specific focus on B cells.

View Article: PubMed Central - PubMed

Affiliation: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill Chapel Hill, NC, USA ; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.

ABSTRACT
As an obligate intracellular parasite, Kaposi sarcoma-associated herpesvirus (KSHV) relies on the host cell machinery to meet its needs for survival, viral replication, production, and dissemination of progeny virions. KSHV is a gammaherpesvirus that is associated with three different malignancies: Kaposi sarcoma (KS), and two B cell lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman's disease. KSHV viral proteins modulate the cellular phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway, which is a ubiquitous pathway that also controls B lymphocyte proliferation and development. We review the mechanisms by which KSHV manipulates the PI3K/AKT/mTOR pathway, with a specific focus on B cells.

No MeSH data available.


Related in: MedlinePlus

Kaposi sarcoma-associated herpesvirus K1 activates PI3K/AKT/mTOR signaling thereby activating protein synthesis and survival pathways, while inhibiting apoptotic pathways. Orange circles denote phosphorylation.
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Figure 1: Kaposi sarcoma-associated herpesvirus K1 activates PI3K/AKT/mTOR signaling thereby activating protein synthesis and survival pathways, while inhibiting apoptotic pathways. Orange circles denote phosphorylation.

Mentions: Various studies describe the extent to which K1 also deregulates normal cellular signaling (Figure 1). The regulatory p85 subunit modulates PI3K activity, and tyrosine-phosphorylation of p85 results in activation of PI3K (Cuevas et al., 2001). K1 expression leads to increased tyrosine phosphorylation of p85, in addition to phosphorylation of Vav and Syk, thus activating signaling networks downstream of these kinases, which have pleiotropic effects on the cell (Lagunoff et al., 1999; Lee et al., 2003; Tomlinson and Damania, 2004). Further, activation of transcription factors downstream of these kinases, for example, NFAT, downstream of Syk signaling, further augments deregulation of cellular signaling and promotes cell survival.


AKTivation of PI3K/AKT/mTOR signaling pathway by KSHV.

Bhatt AP, Damania B - Front Immunol (2013)

Kaposi sarcoma-associated herpesvirus K1 activates PI3K/AKT/mTOR signaling thereby activating protein synthesis and survival pathways, while inhibiting apoptotic pathways. Orange circles denote phosphorylation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3539662&req=5

Figure 1: Kaposi sarcoma-associated herpesvirus K1 activates PI3K/AKT/mTOR signaling thereby activating protein synthesis and survival pathways, while inhibiting apoptotic pathways. Orange circles denote phosphorylation.
Mentions: Various studies describe the extent to which K1 also deregulates normal cellular signaling (Figure 1). The regulatory p85 subunit modulates PI3K activity, and tyrosine-phosphorylation of p85 results in activation of PI3K (Cuevas et al., 2001). K1 expression leads to increased tyrosine phosphorylation of p85, in addition to phosphorylation of Vav and Syk, thus activating signaling networks downstream of these kinases, which have pleiotropic effects on the cell (Lagunoff et al., 1999; Lee et al., 2003; Tomlinson and Damania, 2004). Further, activation of transcription factors downstream of these kinases, for example, NFAT, downstream of Syk signaling, further augments deregulation of cellular signaling and promotes cell survival.

Bottom Line: As an obligate intracellular parasite, Kaposi sarcoma-associated herpesvirus (KSHV) relies on the host cell machinery to meet its needs for survival, viral replication, production, and dissemination of progeny virions.KSHV is a gammaherpesvirus that is associated with three different malignancies: Kaposi sarcoma (KS), and two B cell lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman's disease.We review the mechanisms by which KSHV manipulates the PI3K/AKT/mTOR pathway, with a specific focus on B cells.

View Article: PubMed Central - PubMed

Affiliation: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill Chapel Hill, NC, USA ; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill Chapel Hill, NC, USA.

ABSTRACT
As an obligate intracellular parasite, Kaposi sarcoma-associated herpesvirus (KSHV) relies on the host cell machinery to meet its needs for survival, viral replication, production, and dissemination of progeny virions. KSHV is a gammaherpesvirus that is associated with three different malignancies: Kaposi sarcoma (KS), and two B cell lymphoproliferative disorders, primary effusion lymphoma (PEL) and multicentric Castleman's disease. KSHV viral proteins modulate the cellular phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway, which is a ubiquitous pathway that also controls B lymphocyte proliferation and development. We review the mechanisms by which KSHV manipulates the PI3K/AKT/mTOR pathway, with a specific focus on B cells.

No MeSH data available.


Related in: MedlinePlus