RNA polymerase activity in homotransplanted rat brain tumors initially induced by ethylnitrosourea

1975 ◽  
Vol 32 (1) ◽  
pp. 1-7 ◽  
Author(s):  
D. E. Slagel ◽  
H. Norrell
1971 ◽  
Vol 49 (12) ◽  
pp. 1318-1325 ◽  
Author(s):  
I. A. Menon

Phospholipase A and phospholipase C increased the RNA polymerase activities in presence of Mg2+ or Mn2+ of aggregate enzyme preparation from rat brain. The stimulatory effects were not observed when the RNA polymerase activities were determined in presence of 0.4 M ammonium sulfate, KCl, or NaCl. Trypsin, pronase, and papain were found to enhance the RNA polymerase activity in presence of Mn2+ whereas they had little or no effect on the activity in presence of Mg2+. The phospholipase had relatively less effect on the RNA polymerase activity of frozen and thawed or sonicated aggregate enzyme preparation. Treatment with phospholipase A solubilized approximately 50% of the RNA polymerase. The RNA polymerase activity of brain mitochondria was stimulated by treatment with the phospholipases. The results indicate that phospholipids associated with chromatin and RNA polymerase, as well as those in mitochondria, influence the activity of the RNA polymerases.


1980 ◽  
Vol 85 (2) ◽  
pp. 341-347 ◽  
Author(s):  
B. D. GREENSTEIN

A sensitive, reliable assay of activity of RNA polymerase in purified nuclei from the rat brain is described. The assay measured the incorporation of [3H]guanosine triphosphate into RNA by nuclei. Little incorporation occurred in the presence of α-amanitin (400 ng) suggesting that RNA polymerase B activity was being measured. Preliminary evidence showed that after administration of oestradiol benzoate to 18-day-old female rats RNA polymerase activity was raised in areas of brain known to contain oestrogen receptors.


2021 ◽  
pp. molcanther.MCT-20-0489-A.2020
Author(s):  
Daniel A. R. Heisey ◽  
Sheeba Jacob ◽  
Timonthy L Lochmann ◽  
Richard Kurupi ◽  
Maninderjit S. Ghotra ◽  
...  

1984 ◽  
Vol 4 (1) ◽  
pp. 188-194
Author(s):  
B S Ben-Tzvi ◽  
Y Koltin ◽  
M Mevarech ◽  
A Tamarkin

RNA polymerase activity is associated with the double-stranded RNA virions of Ustilago maydis. The reaction products of the polymerase activity are single-stranded RNA molecules. The RNA molecules synthesized are homologous to the three classes of double-stranded RNA molecules that typify the viral genome. The single-stranded RNA synthesized is released from the virions. The molecular weight of the single-stranded RNA transcripts is about half the size of the double-stranded RNA segments, and thus, it appears that in the in vitro reaction, full-length transcripts can be obtained.


2018 ◽  
Vol 93 (4) ◽  
Author(s):  
Huan Chen ◽  
Yingjuan Qian ◽  
Xin Chen ◽  
Zhiyang Ruan ◽  
Yuetian Ye ◽  
...  

ABSTRACT The life cycle of influenza A virus (IAV) is modulated by various cellular host factors. Although previous studies indicated that IAV infection is controlled by HDAC6, the deacetylase involved in the regulation of PA remained unknown. Here, we demonstrate that HDAC6 acts as a negative regulator of IAV infection by destabilizing PA. HDAC6 binds to and deacetylates PA, thereby promoting the proteasomal degradation of PA. Based on mass spectrometric analysis, Lys(664) of PA can be deacetylated by HDAC6, and the residue is crucial for PA protein stability. The deacetylase activity of HDAC6 is required for anti-IAV activity, because IAV infection was enhanced due to elevated IAV RNA polymerase activity upon HDAC6 depletion and an HDAC6 deacetylase dead mutant (HDAC6-DM; H216A, H611A). Finally, we also demonstrate that overexpression of HDAC6 suppresses IAV RNA polymerase activity, but HDAC6-DM does not. Taken together, our findings provide initial evidence that HDAC6 plays a negative role in IAV RNA polymerase activity by deacetylating PA and thus restricts IAV RNA transcription and replication. IMPORTANCE Influenza A virus (IAV) continues to threaten global public health due to drug resistance and the emergence of frequently mutated strains. Thus, it is critical to find new strategies to control IAV infection. Here, we discover one host protein, HDAC6, that can inhibit viral RNA polymerase activity by deacetylating PA and thus suppresses virus RNA replication and transcription. Previously, it was reported that IAV can utilize the HDAC6-dependent aggresome formation mechanism to promote virus uncoating, but HDAC6-mediated deacetylation of α-tubulin inhibits viral protein trafficking at late stages of the virus life cycle. These findings together will contribute to a better understanding of the role of HDAC6 in regulating IAV infection. Understanding the molecular mechanisms of HDAC6 at various periods of viral infection may illuminate novel strategies for developing antiviral drugs.


1972 ◽  
Vol 11 (11) ◽  
pp. 3105-3110 ◽  
Author(s):  
J.F. Payne ◽  
Arya K. Bal

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