Results 191 to 200 of about 98,603 (254)

Mechanistic coupling of enzymatic activities at the replisome. [PDF]

open access: yesJ Biol Chem
Welikala MU   +3 more
europepmc   +1 more source

Antibody to the RNA-dependent DNA polymerase of mammalian C-type RNA tumor viruses.

open access: yesProceedings of the National Academy of Sciences of the United States of America, 1971
S. Aaronson   +3 more
semanticscholar   +1 more source

Mammalian Proteome Profiling Reveals Readers and Antireaders of Strand‐Symmetric and ‐Asymmetric 5‐Hydroxymethylcytosine‐Modifications in DNA

open access: yesAdvanced Science, EarlyView.
ABSTRACT The cytosine (C) modifications 5‐methylcytosine (mC) and 5‐hydroxymethylcytosine (hmC) are central regulatory elements of mammalian genomes. Both marks occur in double‐stranded DNA in either strand‐symmetric or ‐asymmetric fashion, but it is still poorly understood how this symmetry information is selectively read out by the nuclear proteome ...
Lena Engelhard   +8 more
wiley   +1 more source

3-Cyclic amine derivatives of rifamycin: strong inhibitors of the DNA polymerase activity of RNA tumor viruses.

open access: yesProceedings of the National Academy of Sciences of the United States of America, 1972
M. Green, J. Bragdon, A. Rankin
semanticscholar   +1 more source

Small Nucleolar RNA Snord17 Promotes Self‐Renewal of Intestinal Stem Cells through Yy2 mRNA Export and Tead4 Activation

open access: yesAdvanced Science, EarlyView.
Snord17, through interaction with Thoc3, promotes nuclear export and translation of Yy2 mRNA in Snord17+/+ ISCs. The Yy2 protein subsequently binds the Tead4 promoter to promote its transcription, activating Hippo signaling, which is essential for ISC maintenance.
Peikang Zhang   +10 more
wiley   +1 more source

Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting R‐Loop Accumulation and DNA Repair Deficiencies

open access: yesAdvanced Science, EarlyView.
ARID1A, a SWI/SNF complex component, is frequently mutated in colorectal cancer (CRC). CRC with ARID1A/TP53 concurrent mutations shows marked sensitivity to WEE1 inhibition. ARID1A loss induces R‐loop‐mediated replication stress, impairs ATF3 transcription, and amplifies WEE1i‐induced DNA damage, suggesting a promising therapeutic vulnerability ...
Chi Zhang   +17 more
wiley   +1 more source

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