EBV LMP1: New and shared pathways to NF-κB activation

Lavorgna, Alfonso; Harhaj, Edward W.

doi:10.1073/pnas.1121357109

Cited by 36 publications

(32 citation statements)

References 18 publications

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“…LMP-1 suppresses the induction of ATF3, a transcription factor associated with TGF-b, and inhibits BAX activity by inducing NF-kB activity. 17 EBV produces BHRF-1, a viral BCL-2 homolog, which binds to BAK and the BH3-only proteins PUMA, BID, and BIM. By targeting these BAX/BAK activators, BHRF-1 prevents TGF-b-mediated apoptosis.…”

Section: Pathogenesis and Cell Of Originmentioning

confidence: 99%

The biology and treatment of plasmablastic lymphoma

Castillo

Bibas

Miranda

2015

Blood

371

543

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Plasmablastic lymphoma (PBL) is an aggressive lymphoma commonly associated with HIV infection. However, PBL can also be seen in patients with other immunodeficiencies as well as in immunocompetent individuals. Because of its distinct clinical and pathological features, such as lack of expression of CD20, plasmablastic morphology, and clinical course characterized by early relapses and subsequent chemotherapy resistance, PBL can represent a diagnostic and therapeutic challenge for pathologists and clinicians alike. Despite the recent advances in the therapy of HIV-associated and aggressive lymphomas, patients with PBL for the most part have poor outcomes. The objectives of this review are to summarize the current knowledge on the epidemiology, biology, clinical and pathological characteristics, differential diagnosis, therapy, prognostic factors, outcomes, and potential novel therapeutic approaches in patients with PBL and also to increase the awareness toward PBL in the medical community.

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Section: Pathogenesis and Cell Of Originmentioning

confidence: 99%

The biology and treatment of plasmablastic lymphoma

Castillo

Bibas

Miranda

2015

Blood

371

543

View full text Add to dashboard Cite

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“…This is a well-known oncoprotein that plays a key role in the immortalization of EBV-infected cells [99]. Not surprisingly, LMP-1 has been extensively studied and shown to function as a constitutively activated receptor, signaling through the TRAF pathway leading to the activation of the master transcription factor, NFκB [100,101]. LMP-2A is also an EBV latent protein expressed on the plasma membrane of latently infected cells [102].…”

Section: Role Of Exosomes In Viral Pathogenesismentioning

confidence: 99%

Exosomes and Their Role in Viral Infections

Khan¹,

Ahmed²,

Philip³

2017

Novel Implications of Exosomes in Diagnosis and Treatment of Cancer and Infectious Diseases

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Exosomes are excretory nano-vesicles that are formed by the cell's endocytic system and shed from the surface of almost all types of cells. These tiny extracellular vesicles, once thought to be "garbage bags for cells," carry a wide variety of molecules of cellular origin, including proteins, lipids, and RNAs, that are selectively incorporated during the formation of exosomes. Exosomes are now known to play a central role in several important biological processes such as cellular communication, intercellular transfer of bioactive molecules, and immune modulation. Recent advances in the field have shown that a number of animal viruses can exploit the exosomal pathway by incorporating specific cellular or viral factors within exosomes, in order to modulate the cellular microenvironment and influence downstream processes such as host immunity and virus spread. In this chapter, we provide an overview of our current understanding of exosome biogenesis and how this normal physiological process is hijacked by some pathogenic viruses. Viral components that appear to be selectively incorporated into exosomes and the potential role of these exosomes in viral pathogenesis are discussed. Identifying viral signatures in exosomes and their mode of action is fundamental for any future diagnostic and therapeutic strategies for viral infections.

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“…lMP1 is a 386 amino acid transmembrane glycoprotein, which consists of a short cytoplasmic n-terminal domain (residues 1-23), six transmembrane domains (residues 24-186), and a long cytoplasmic c-terminal domain (residues 187-386), which is known as the carboxyl terminal activation region (cTar) (3). currently, three cTars have been reported, cTar1 (residues 194-232), cTar2 (residues 351-386) and cTar3 (residues 275-330) (4). cTar1 engages tumor necrosis factor receptor-associated factors to induce low-level nuclear factor-κB (nF-κB) activation (5).…”

Section: Introductionmentioning

confidence: 99%

Carboxyl terminal activating region 3 of latent membrane protein 1 encoded by the Epstein‑Barr virus regulates cell proliferation and protein expression in NP69 cells

Zhang

et al. 2019

Mol Med Report

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in the present study, the mechanism by which carboxyl terminal activating region 3 (cTar3) of latent membrane protein 1 (lMP1), encoded by the epstein-Barr virus, regulated cell proliferation and protein expression was investigated in the nasopharyngeal epithelial cell line nP69. The deletion mutant lMP1 (lMP1 Δ232-351 ; amino acid residues including 232-351 codons in cTar3 deleted) was generated by polymerase chain reaction. an nP69-lMP1 Δ232-351 cell line was established by retroviral infection. Finally, cell proliferation and protein expression of nP69 cells expressing lMP1 Δ232-351 were examined using a cell growth curve and western blot analysis. The results demonstrated: i) The proliferation of nP69-lMP1 Δ232-351 cells was significantly decreased compared with cells expressing wild type lMP1 (lMP1 WT ; n=3; P<0.05); ii) 17 proteins exhibited differential protein expression (>2-fold change) in nP69-lMP1 Δ232-351 cells compared with nP69-lMP1 WT cells; and iii) lMP1 WT was involved in activating the Janus kinase 3 (JaK3) promoter and regulating the expression of JaK3 protein, while lMP1 Δ232-351 was almost defective in ability to activate the JaK promoter. These results suggested that lMP1-cTar3 may be an important functional domain for regulating cell proliferation and protein expression in nasopharyngeal epithelial cells.

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EBV LMP1: New and shared pathways to NF-κB activation

Cited by 36 publications

References 18 publications

The biology and treatment of plasmablastic lymphoma

The biology and treatment of plasmablastic lymphoma

Exosomes and Their Role in Viral Infections

Carboxyl terminal activating region 3 of latent membrane protein 1 encoded by the Epstein‑Barr virus regulates cell proliferation and protein expression in NP69 cells

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