EC Number   |
General Information |
Reference |
|---|
   3.1.26.13 | evolution |
RNase H acts as gene modifier, driver of evolution and antiviral defense, overview |
750633 |
| 3.1.26.13 | evolution |
the N-terminal amino acid residue of HIV-1 RNase H is highly conserved |
751426 |
| 3.1.26.13 | malfunction |
an HIV-1 mutant can tolerate an about 10fold higher RNase H activity |
752320 |
| 3.1.26.13 | malfunction |
antiviral activity of 2-hydroxy-4-methoxycarbonylisoquinoline-1,3(2H,4H)-dione is probably due to the RNase H inhibition |
715859 |
| 3.1.26.13 | malfunction |
effect of N-terminal deletion on monomer-dimer interconversion kinetics, overview |
751727 |
| 3.1.26.13 | malfunction |
identification of nucleoside reverse transcriptase inhibitor (NRTI) treatment-related mutations in RNase H of HIV-1 subtype C, overview |
752326 |
| 3.1.26.13 | malfunction |
patients treated with nucleoside reverse transcriptase inhibitors develop classical patterns of resistance-associated mutations in the pol domain. Thymidine analogue mutations, TAMs, arise with zidovudine and stavudine treatment, which encompass M41L, D67N, K70R, L210W, T215F/Y, and K219Q/E/N. Different patterns of thymidine analogue mutations accumulate in patients, which segregate into two distinct pathways named TAM-1 and TAM-2. The TAM-1 pathway includes M41L, L210W and T215Y, whereas the TAM-2 pathway includes D67N, K70R, T215F and K219Q/E/N |
-, 716993 |
| 3.1.26.13 | malfunction |
PEGylation as a tool for engineering the M-MuLV RT derivative deficient in RNase H activity, overview |
716354 |
| 3.1.26.13 | malfunction |
RNase H N-terminal mutations impact intravirion protein levels and viral infectivity. Reverse transcriptase (RT) with an RNaseHN-terminal mutation is still degraded in the absence of active viral protease |
751426 |
| 3.1.26.13 | malfunction |
RNase H-deficient HIV-1 reverse transcriptase shows altered error specificity during DNA-dependent DNA synthesis |
730494 |
