Dysregulation of the Polo-Like Kinase Pathway in CD4
            <sup>+</sup>
            T Cells Is Characteristic of Pathogenic Simian Immunodeficiency Virus Infection

Boštík, Pavel; Dodd, Geraldine L.; Villinger, François; Mayne, Ann E.; Ansari, Aftab A.

doi:10.1128/jvi.78.3.1464-1472.2004

Cited by 31 publications

(20 citation statements)

References 55 publications

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“…rhesus macaques) and nonpathogenic (i.e., SMs) SIV infection has shown that a variety of cell cycle perturbations is observed in apoptosis-sensitive T cells derived from the peripheral blood and lymph nodes of macaques infected with SIV and progressing to AIDS, while normal cell cycle regulation is observed in apoptosis-resistant T cells from naturally SIVinfected SMs that do not progress to AIDS. 128 Taken together, these findings suggest that during pathogenic HIV and SIV infections (but not during nonpathogenic SIV infection of natural hosts), the presence of cell cycle dysregulation is involved in determining the abnormal susceptibility to apoptosis of T lymphocytes. 124 The Interaction between the Envelope Glycoprotein and CD4/coreceptors is a Crucial Factor in the Pathogenesis of AIDS HIV-1 infection can cause apoptosis via a variety of mechanisms, some of which rely directly on the intricate interaction between the virus and the host cells, and some of which act indirectly through activation of the host's inflammatory reaction and immune system activation.…”

Section: Cell Cycle Dysregulationmentioning

confidence: 79%

Apoptosis in SIV infection

et al. 2005

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Section: Cell Cycle Dysregulationmentioning

confidence: 79%

Apoptosis in SIV infection

et al. 2005

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“…Total RNA was extracted with TRIZOL (Invitrogen) and real-time PCR was performed with MyiQ Single-Color Real-Time PCR Detection System (Bio-Rad) as described [37]. Briefly, cDNA samples were subjected to real-time PCR in an iCycler (Bio-Rad) and SYBR Green fluorescence quantification (PE Applied Biosystems; Foster City, CA, USA).…”

Section: Real Time-polymerase Chain Reaction (Real Time-pcr)mentioning

confidence: 99%

Id-1 regulates Bcl-2 and Bax expression through p53 and NF-κB in MCF-7 breast cancer cells

Kim

Chung

Kim

et al. 2007

Breast Cancer Res Treat

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Although increasing evidence supports the protective role of inhibitor of differentiation and DNA binding-1 (Id-1) against anticancer drug-induced apoptosis, the underlying molecular mechanisms seem to vary depending on the tumor system. Here, we examined the direct role of Id-1 in MCF-7 breast cancer cells by ectopically overexpressing Id-1 under serum-free condition, where the endogenous Id-1 expression was suppressed. Id-1 expression resulted in increased number of viable cells, reduced Bax expression, enhanced Bcl-2 expression, but no change in Bcl-xL expression. The expression of nuclear factor-kappaB (NF-kappaB) was augmented, while those of p53 and IkappaB were reduced. Such changes in p53 and NF-kappaB pathways were also functional, as assessed by real-time polymerase chain reactions and reporter assays of their known downstream targets, p21 and Il-6, as well as Bax and Bcl-2 genes. Finally, Id-1 played a protective role against taxol-induced apoptosis in breast cancer cells as assessed by MTT assay and apoptotic cell count upon taxol treatment (0-200 nM). Reduced Bax expression and enhanced Bcl-2 expression by Id-1 were also noted in the presence of taxol. Taken together, we present a molecular mechanism where Id-1 regulates p53 and NF-kappaB pathways, which in turn regulates Bax and Bcl-2 genes, thus providing a survival advantage under exogenous stress such as serum-free or taxol treatment in MCF-7 breast cancer cells. In this regard, inactivation of Id-1 may provide a potential therapeutic strategy leading to inhibition of breast cancer progression and anti-cancer drug resistance.

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“…Our laboratory has been involved with studies of the mechanisms of pathogenesis of lentivirus infection using the simian immunodeficiency virus (SIV) infected non-human primate model (25–27). We and others have shown that, similar to HIV infection in humans, there are phenotypic changes and functional impairment in the NK cell population that occur during both acute and chronic phases of SIV infection in rhesus macaques (RMs) (28, 29).…”

mentioning

confidence: 99%

Decreased NK Cell Frequency and Function Is Associated with Increased Risk of KIR3DL Allele Polymorphism in Simian Immunodeficiency Virus-Infected Rhesus Macaques with High Viral Loads

Boštík

Kobkitjaroen

Tang

et al. 2009

The Journal of Immunology

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NK cells have been established as an important effector of innate immunity in a variety of viral infections. In HIV-1 infection in humans, alterations of NK cell function, frequency, and expression of various NK receptors have been reported to be associated with differential dynamics of disease progression. Expression of certain alleles of KIR3DL and KIR3DS receptors on NK cells was shown to correlate with levels of virus replication. In the SIV-infected rhesus macaque (RM) model of AIDS, several families of killer inhibitory Ig-related receptors (KIR receptors) corresponding to their human counterparts have been characterized, but only at the level of individual sequence variants. Here we define 14 different alleles of KIR3DL expressed among 38 SIV-infected RM, characterized by either high or low levels of SIV replication, by analyzing multiple sequences from individual animals and show an unequal distribution of certain alleles in these cohorts. High levels of SIV replication were associated with significant increases in KIR3DL mRNA levels in addition to decreases in both the frequency and function of NK cells in these animals. The higher frequency of inheritance of two KIR3DL alleles characterized by a single nucleotide polymorphism 159 H/Q was associated with RM that exhibited high plasma viral load. This data for the first time defines multiple alleles of KIR3DL in RM and shows an association between virus control, NK cell function and genetic polymorphisms of KIR receptors.

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Dysregulation of the Polo-Like Kinase Pathway in CD4 ⁺ T Cells Is Characteristic of Pathogenic Simian Immunodeficiency Virus Infection

Abstract: CD4؉ T-cell dysfunction highlighted by defects within the intracellular signaling cascade and cell cycle has long been characterized as a direct and/or indirect consequence of human immunodeficiency virus (

Cited by 31 publications

References 55 publications

Apoptosis in SIV infection

Apoptosis in SIV infection

Id-1 regulates Bcl-2 and Bax expression through p53 and NF-κB in MCF-7 breast cancer cells

Decreased NK Cell Frequency and Function Is Associated with Increased Risk of KIR3DL Allele Polymorphism in Simian Immunodeficiency Virus-Infected Rhesus Macaques with High Viral Loads

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Dysregulation of the Polo-Like Kinase Pathway in CD4 + T Cells Is Characteristic of Pathogenic Simian Immunodeficiency Virus Infection

Abstract: CD4؉ T-cell dysfunction highlighted by defects within the intracellular signaling cascade and cell cycle has long been characterized as a direct and/or indirect consequence of human immunodeficiency virus (

Cited by 31 publications

References 55 publications

Apoptosis in SIV infection

Apoptosis in SIV infection

Id-1 regulates Bcl-2 and Bax expression through p53 and NF-κB in MCF-7 breast cancer cells

Decreased NK Cell Frequency and Function Is Associated with Increased Risk of KIR3DL Allele Polymorphism in Simian Immunodeficiency Virus-Infected Rhesus Macaques with High Viral Loads

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Dysregulation of the Polo-Like Kinase Pathway in CD4 ⁺ T Cells Is Characteristic of Pathogenic Simian Immunodeficiency Virus Infection