The proximal tubule has a remarkable capacity for repair after acute injury, but the cellular
lineage and molecular mechanisms underlying this repair response are incompletely …

The rnhAB mutant Escherichia coli, deficient in two RNase H enzymes that remove both R-loops
and incorporated ribonucleotides (rNs) from DNA, grow slowly, suggesting …

Half of hereditary nonpolyposis colon cancer kindreds harbor mutations that inactivate MutLα
(MLH1•PMS2 heterodimer). MutLα is required for mismatch repair, but its function in this …

MutLα (MLH1–PMS2) is a latent endonuclease that is activated in a mismatch-, MutSα-,
proliferating cell nuclear antigen (PCNA)-, replication factor C (RFC)-, and ATP-dependent …

The homeobox transcription factor Meis1 is required for mammalian development, and its
overexpression plays a role in tumorigenesis, especially leukemia. Meis1 is known to be …

MutL homologs are crucial for mismatch repair and genetic stability, but their function is not
well understood. Human MutLα (MLH1-PMS2 heterodimer) harbors a latent endonuclease …

Recovery of cardiac function is the holy grail of heart failure therapy yet is infrequently
observed and remains poorly understood. In this study, we performed single-nucleus RNA …

Bidirectional mismatch repair directed by a strand break located 3′ or 5′ to the mispair has
been reconstituted using seven purified human activities: MutSα, MutLα, EXOI, replication …

Mismatch repair contributes to genetic stability, and inactivation of the mammalian pathway
leads to tumor development. Mismatch correction occurs by an excision-repair mechanism …

MutLα, the heterodimeric eukaryotic MutL homolog, is required for DNA mismatch repair (MMR)
in vivo. It has been suggested that conformational changes, modulated by adenine …