scholarly journals Down regulation of lactate dehydrogenase initiates apoptosis in HeLa and MCF-7 cancer cells through increased voltage-dependent anion channel protein and inhibition of BCL2

Oncotarget ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 923-935
Author(s):  
Suhail Al-Salam ◽  
Karthishwaran Kandhan ◽  
Manjusha Sudhadevi
Gene ◽  
2003 ◽  
Vol 317 ◽  
pp. 111-115 ◽  
Author(s):  
Marco Sardiello ◽  
Gaetano Tripoli ◽  
Marta Oliva ◽  
Federica Santolamazza ◽  
Roberta Moschetti ◽  
...  

PROTEOMICS ◽  
2004 ◽  
Vol 4 (5) ◽  
pp. 1335-1340 ◽  
Author(s):  
Sabrina Liberatori ◽  
Benito Canas ◽  
Chiara Tani ◽  
Luca Bini ◽  
Giuseppe Buonocore ◽  
...  

2007 ◽  
Vol 67 (11) ◽  
pp. 1533-1545 ◽  
Author(s):  
Sunji Lee ◽  
Hung-Tat Leung ◽  
Eunju Kim ◽  
Jeyoun Jang ◽  
Eunsung Lee ◽  
...  

2019 ◽  
Vol 93 (12) ◽  
Author(s):  
Ying Zhong ◽  
Xiaoqian Tang ◽  
Xiuzhen Sheng ◽  
Jing Xing ◽  
Wenbin Zhan

ABSTRACTIn previous research, a 27.8-kDa protein in flounderParalichthys olivaceusgill (FG) cells was identified as a putative cellular receptor (27.8R), which mediated lymphocystis disease virus (LCDV) infection via interaction with a 32-kDa viral attachment protein (VAP) of LCDV, and monoclonal antibodies (MAbs) against 27.8R and 32-kDa VAP were developed. In this study, the 27.8R was identified as voltage-dependent anion channel protein 2 (VDAC2) and receptor of activated protein C kinase 1 (RACK1) of flounder. Recombinant VDAC2 (rVDAC2) and RACK1 (rRACK1) were obtained by prokaryotic expression, and rabbit anti-VDAC2/RACK1 polyclonal antibodies were prepared. The rVDAC2, rRACK1, and 27.8-kDa proteins in FG cells were recognized by anti-27.8R MAbs and anti-VDAC2/RACK1 polyclonal antibodies simultaneously. Preincubation of FG cells with anti-VDAC2/RACK1 polyclonal antibodies significantly decreased the percentages of LCDV-infected cells and LCDV copy numbers, blocked virus infection, and delayed the development of cytopathic effect. The mRNA expressions of VDAC2 and RACK1 in FG cells were upregulated to maximum levels 12 h and 48 h after LCDV infection, respectively. VDAC2/RACK1 knockdown through short interfering RNA (siRNA) significantly reduced VDAC2/RACK1 expression and LCDV copy numbers in FG cells compared with negative controls, while VDAC2/RACK1 expression on LCDV-nonpermissive epithelial papillosum cells (EPCs) conferred susceptibility to LCDV infection, indicating the VDAC2 and RACK1 were sufficient to allow LCDV entry and infection. All these results collectively showed that VDAC2 and RACK1 function as receptors for LCDV entry and infection.IMPORTANCELymphocystis disease virus (LCDV) is the causative agent of lymphocystis disease in fish, which has caused huge economic losses to the aquaculture industry worldwide, but the molecular mechanism underlying the LCDV-host interaction remains unclear. Here, the 27.8-kDa putative cellular receptor for LCDV was identified as voltage-dependent anion channel protein 2 (VDAC2) and receptor of activated protein C kinase 1 (RACK1), and our results revealed that VDAC2 and RACK1 expression was sufficient to allow LCDV entry and that they are functional receptors that initiate LCDV infection for the first time, which leads to a better understanding of the molecular mechanism underlying LCDV infection and virus-host interactions.


2007 ◽  
Vol 67 (12) ◽  
pp. 1686-1686
Author(s):  
Sunji Lee ◽  
Hung-Tat Leung ◽  
Eunju Kim ◽  
Jeyoun Jang ◽  
Eunsung Lee ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document