Inhibition of SIRT1 by HIV-1 viral protein Tat results in activation of p53 pathway

Thakur, Basant Kumar; Chandra, Angelika; Dittrich, Tino; Welte, Karl; Prakash, Chandra

doi:10.1016/j.bbrc.2012.06.084

Cited by 29 publications

(31 citation statements)

References 35 publications

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“…Interestingly, the mTOR pathway has been reported to contribute to the pathogenesis of diabetic and HIV-associated nephropathy (25,26). Moreover, the effector molecules of these entities-glucose and HIVhave also been reported to activate both kidney cell mTOR and p53 pathways (23,35,36,46). However, there are no data on cross talk between mTOR and p53 in the development of these diseases.…”

Section: Discussionmentioning

confidence: 99%

mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN

Rai

Plagov

Lan

et al. 2013

American Journal of Physiology-Renal Physiology

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Section: Discussionmentioning

confidence: 99%

mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN

Rai

Plagov

Lan

et al. 2013

American Journal of Physiology-Renal Physiology

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“…A portion of the current research efforts focus on finding novel host-based therapies that can provide viral inhibition in tandem with protection of cells from apoptosis. Cytoprotective effects are desirable in order to protect already depleted cell populations and to counteract detrimental effects of viral proteins, such as Tat and gp120 (Env), which are normally generated during infection (6)(7)(8)(9)(10)(11).…”

mentioning

confidence: 99%

“…The Tat/TAR complex is able to recruit various critical host cell factors, such as the pTEF-b complex (Cdk9/Cyclin T1), to the RNA polymerase II complex that occupies the LTR (12)(13)(14)(15)(16)(17)(18)(19). Due to its small size and stretch of basic residues, Tat can be secreted into the extracellular environment, where it exerts various functional effects on bystander cells (8,(20)(21)(22)(23)(24)(25)(26). The neurotoxic effects of HIV-1 are largely attributed to the Tat and gp120 proteins (27,28).…”

mentioning

confidence: 99%

Novel Neuroprotective GSK-3β Inhibitor Restricts Tat-Mediated HIV-1 Replication

Guendel

Iordanskiy

Duyne

et al. 2014

J Virol

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“…Investigations into the relationship between Tat protein and SIRT1, which plays a role in the activation of the p53 pathway leading to apoptosis in T-cells, [236,237,238,239,240,241,242] showed that Tat is able to inactivate SIRT1, thereby, activating the p53 pathway resulting in T-cell depletion [80,236]. This implies that SIRT1 could be used as a potential therapeutic target for inhibiting apoptosis [236].…”

Section: Therapeutic Targets: Targeting Apoptotic Pathwaysmentioning

confidence: 99%

“…This implies that SIRT1 could be used as a potential therapeutic target for inhibiting apoptosis [236]. …”

Section: Therapeutic Targets: Targeting Apoptotic Pathwaysmentioning

confidence: 99%

Human Immunodeficiency Virus-1 (HIV-1)-Mediated Apoptosis: New Therapeutic Targets

Mbita

Hull

Dlamini

2014

Viruses

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HIV has posed a significant challenge due to the ability of the virus to both impair and evade the host’s immune system. One of the most important mechanisms it has employed to do so is the modulation of the host’s native apoptotic pathways and mechanisms. Viral proteins alter normal apoptotic signaling resulting in increased viral load and the formation of viral reservoirs which ultimately increase infectivity. Both the host’s pro- and anti-apoptotic responses are regulated by the interactions of viral proteins with cell surface receptors or apoptotic pathway components. This dynamic has led to the development of therapies aimed at altering the ability of the virus to modulate apoptotic pathways. These therapies are aimed at preventing or inhibiting viral infection, or treating viral associated pathologies. These drugs target both the viral proteins and the apoptotic pathways of the host. This review will examine the cell types targeted by HIV, the surface receptors exploited by the virus and the mechanisms whereby HIV encoded proteins influence the apoptotic pathways. The viral manipulation of the hosts’ cell type to evade the immune system, establish viral reservoirs and enhance viral proliferation will be reviewed. The pathologies associated with the ability of HIV to alter apoptotic signaling and the drugs and therapies currently under development that target the ability of apoptotic signaling within HIV infection will also be discussed.

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Inhibition of SIRT1 by HIV-1 viral protein Tat results in activation of p53 pathway

Cited by 29 publications

References 35 publications

mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN

mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN

Novel Neuroprotective GSK-3β Inhibitor Restricts Tat-Mediated HIV-1 Replication

Human Immunodeficiency Virus-1 (HIV-1)-Mediated Apoptosis: New Therapeutic Targets

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