Activation of JNK-dependent pathway is required for HIV viral protein R-induced apoptosis in human monocytic cells: involvement of antiapoptotic BCL2 and c-IAP1 genes (Q40198408)

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scientific article published on 11 December 2006

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English	Activation of JNK-dependent pathway is required for HIV viral protein R-induced apoptosis in human monocytic cells: involvement of antiapoptotic BCL2 and c-IAP1 genes	scientific article published on 11 December 2006

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

retracted paper

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Dataset for "Continued use of retracted papers: Temporal trends in citations and (lack of) awareness of retractions shown in citation contexts in biomedicine"

Continued use of retracted papers: Temporal trends in citations and (lack of) awareness of retractions shown in citation contexts in biomedicine

Activation of JNK-dependent pathway is required for HIV viral protein R-induced apoptosis in human monocytic cells: involvement of antiapoptotic BCL2 and c-IAP1 genes (English)

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

author name string

Sasmita Mishra

1

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

Jyoti P Mishra

2

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

Ashok Kumar

3

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

language of work or name

0 references

publication date

11 December 2006

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

Journal of Biological Chemistry

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Europe PubMed Central

PubMed publication ID

18 September 2017

282

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

7

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

4288-4300

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

Molecular mechanisms of apoptosis in the cells of the immune system in human aging

1 reference

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Modulating apoptosis as a target for effective therapy

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Lentiviral delivery of HIV-1 Vpr protein induces apoptosis in transformed cells

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HIV-1 Vpr displays natural protein-transducing properties: implications for viral pathogenesis.

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The cationic amphipathic alpha-helix of HIV-1 viral protein R (Vpr) binds to nucleic acids, permeabilizes membranes, and efficiently transfects cells.

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HIV-1 Vpr induces apoptosis through caspase 9 in T cells and peripheral blood mononuclear cells

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The HIV-1 viral protein R induces apoptosis via a direct effect on the mitochondrial permeability transition pore

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NMR structure of the HIV-1 regulatory protein VPR

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Expression of the inhibitor of apoptosis (IAP) family members in human neutrophils: up-regulation of cIAP2 by granulocyte colony-stimulating factor and overexpression of cIAP2 in chronic neutrophilic leukemia

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HIV-1 Nef promotes survival of TF-1 macrophages by inducing Bcl-XL expression in an extracellular signal-regulated kinase-dependent manner

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The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis

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IL-7 inhibits dexamethasone-induced apoptosis via Akt/PKB in mature, peripheral T cells

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Mono- and multisite phosphorylation enhances Bcl2's antiapoptotic function and inhibition of cell cycle entry functions

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NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation

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Gene promoter of apoptosis inhibitory protein IAP2: identification of enhancer elements and activation by severe hypoxia

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Control of mitosis by changes in the subcellular location of cyclin-B1-Cdk1 and Cdc25C

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Activation of the ATR-mediated DNA damage response by the HIV-1 viral protein R.

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Vpr protein of human immunodeficiency virus type 1 binds to 14-3-3 proteins and facilitates complex formation with Cdc25C: implications for cell cycle arrest

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Identifiers

10.1074/JBC.M608307200

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

18 September 2017

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