Detergent-induced activation of the hepatitis C virus genotype 1b RNA polymerase

Weng, Leiyun; Kohara, Michinori; Wakita, Takaji; Shimotohno, Kunitada; Toyoda, Tetsuya

doi:10.1016/j.gene.2012.01.044

Cited by 4 publications

(4 citation statements)

References 47 publications

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“…In particular, recent studies have shown that cisplatin, a DNA damage-inducing platinum-based drug, increases the expression of PARP1 during kidney injury. PARP-initiated ATP depletion as well as generation of oxidative stress products causes nephrotoxicity by enhancing necrosis 26 . Cisplatin enhances necrotic cell death through the activation of PARP1 in human (HK-2), mouse (MCT), and pig (LLC-PK1) kidney proximal tubular cells 27 .…”

mentioning

confidence: 99%

Doxorubicin-induced necrosis is mediated by poly-(ADP-ribose) polymerase 1 (PARP1) but is independent of p53

Shin

Kwon

Lee

et al. 2015

Sci Rep

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Necrosis, unregulated cell death, is characterized by plasma membrane rupture as well as nuclear and cellular swelling. However, it has recently been reported that necrosis is a regulated form of cell death mediated by poly-(ADP-ribose) polymerase 1 (PARP1). PARP1 is thought to mediate necrosis by inducing DNA damage, although this remains unconfirmed. In this study, we examined the mechanisms of PARP1-mediated necrosis following doxorubicin (DOX)-induced DNA damage in human kidney proximal tubular (HK-2) cells. DOX initiated DNA damage response (DDR) and upregulated PARP1 and p53 expression, resulting in morphological changes similar to those observed during necrosis. Additionally, DOX induced mitochondrial hyper-activation, as evidenced by increased mitochondrial respiration and cytosolic ATP (cATP) production. However, DOX affected mitochondrial mass. DOX-induced DNA damage, cytosolic reactive oxygen species (cROS) generation, and mitochondrial hyper-activation decreased in cells with inhibited PARP1 expression, while generation of nitric oxide (NO) and mitochondrial ROS (mROS) remained unaffected. Moreover, DOX-induced DNA damage, cell cycle changes, and oxidative stress were not affected by p53 inhibition. These findings suggest that DNA damage induced necrosis through a PARP1-dependent and p53-independent pathway.

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mentioning

confidence: 99%

Doxorubicin-induced necrosis is mediated by poly-(ADP-ribose) polymerase 1 (PARP1) but is independent of p53

Shin

Kwon

Lee

et al. 2015

Sci Rep

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“…The surfactant at micellar and post-micellar concentrations has, however, exhibited cooperative binding toC9W. Many other globular proteins also possess altered structure and shape upon binding non-ionic surfactants including TX-100 [ 27 – 29 , 43 , 48 – 50 ].…”

Section: Discussionmentioning

confidence: 99%

“…Several proteins (including transcription regulator), like rSarA, have shown a higher biological activity in the solution containing TX-100 [ 29 , 51 – 54 ]. Molecules of the non-ionic surfactant usually interact with proteins using their respective hydrophobic regions [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

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A Surfactant-Induced Functional Modulation of a Global Virulence Regulator from Staphylococcus aureus

et al. 2016

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Triton X-100 (TX-100), a useful non-ionic surfactant, reduced the methicillin resistance in Staphylococcus aureus significantly. Many S. aureus proteins were expressed in the presence of TX-100. SarA, one of the TX-100-induced proteins, acts as a global virulence regulator in S. aureus. To understand the effects of TX-100 on the structure, and function of SarA, a recombinant S. aureus SarA (rSarA) and its derivative (C9W) have been investigated in the presence of varying concentrations of this surfactant using various probes. Our data have revealed that both rSarA and C9W bind to the cognate DNA with nearly similar affinity in the absence of TX-100. Interestingly, their DNA binding activities have been significantly increased in the presence of pre-micellar concentration of TX-100. The increase of TX-100 concentrations to micellar or post-micellar concentration did not greatly enhance their activities further. TX-100 molecules have altered the secondary and tertiary structures of both proteins to some extents. Size of the rSarA-TX-100 complex appears to be intermediate to those of rSarA and TX-100. Additional analyses show a relatively moderate interaction between C9W and TX-100. Binding of TX-100 to C9W has, however, occurred by a cooperative pathway particularly at micellar and higher concentrations of this surfactant. Taken together, TX-100-induced structural alteration of rSarA and C9W might be responsible for their increased DNA binding activity. As TX-100 has stabilized the somewhat weaker SarA-DNA complex effectively, it could be used to study its structure in the future.

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Different mechanisms of hepatitis C virus RNA polymerase activation by cyclophilin A and B in vitro

Weng

Tian

Gao

et al. 2012

Biochimica et Biophysica Acta (BBA) - General Subjects

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Detergent-induced activation of the hepatitis C virus genotype 1b RNA polymerase

Cited by 4 publications

References 47 publications

Doxorubicin-induced necrosis is mediated by poly-(ADP-ribose) polymerase 1 (PARP1) but is independent of p53

Doxorubicin-induced necrosis is mediated by poly-(ADP-ribose) polymerase 1 (PARP1) but is independent of p53

A Surfactant-Induced Functional Modulation of a Global Virulence Regulator from Staphylococcus aureus

Different mechanisms of hepatitis C virus RNA polymerase activation by cyclophilin A and B in vitro

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