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Literature DB >> 32573829

A stapled POL κ peptide targets REV1 to inhibit mutagenic translesion synthesis.

Nimrat Chatterjee¹, Sanjay D'Souza^1,2, Mohammad Shabab¹, Cynthia A Harris¹, Gerard J Hilinski³, Gregory L Verdine⁴, Graham C Walker^1,5.

Abstract

Stapled α-helical RIR (Rev1-interacting region) peptides of DNA POL κ bind more effectively to the RIR-interface of the C-terminal recruitment domain of the translesion synthesis DNA polymerase Rev1 than unstapled peptide. The tightest-binding stapled peptide translocates into cells and enhances the cytotoxicity of DNA damaging agents while reducing mutagenesis. Drugs with these characteristics could potentially serve as adjuvants to improve chemotherapy and reduce acquired resistance by inhibiting Rev1-dependent mutagenic translesion synthesis.

Entities: CellLine Chemical Disease Gene Mutation Species

Keywords: chemoresistance; cytotoxicity; mutagenesis; staple peptide; translesion synthesis (TLS)

Mesh：

Substances：

Year: 2020 PMID： 32573829 PMCID： PMC8057520 DOI： 10.1002/em.22395

Source DB: PubMed Journal: Environ Mol Mutagen ISSN： 0893-6692 Impact factor: 3.216

19 in total

1. Stapled peptides for intracellular drug targets.

Authors: Gregory L Verdine; Gerard J Hilinski
Journal: Methods Enzymol Date: 2012 Impact factor: 1.600

2. A Small Molecule Targeting Mutagenic Translesion Synthesis Improves Chemotherapy.

Authors: Jessica L Wojtaszek; Nimrat Chatterjee; Javaria Najeeb; Azucena Ramos; Minhee Lee; Ke Bian; Jenny Y Xue; Benjamin A Fenton; Hyeri Park; Deyu Li; Michael T Hemann; Jiyong Hong; Graham C Walker; Pei Zhou
Journal: Cell Date: 2019-06-06 Impact factor: 41.582

3. XRCC1 interaction with the REV1 C-terminal domain suggests a role in post replication repair.

Authors: Scott A Gabel; Eugene F DeRose; Robert E London
Journal: DNA Repair (Amst) Date: 2013-12

Review 4. Targeting the Translesion Synthesis Pathway for the Development of Anti-Cancer Chemotherapeutics.

Authors: Dmitry M Korzhnev; M Kyle Hadden
Journal: J Med Chem Date: 2016-07-19 Impact factor: 7.446

5. Interaction between the Rev1 C-Terminal Domain and the PolD3 Subunit of Polζ Suggests a Mechanism of Polymerase Exchange upon Rev1/Polζ-Dependent Translesion Synthesis.

Authors: Yulia Pustovalova; Mariana T Q Magalhães; Sanjay D'Souza; Alessandro A Rizzo; George Korza; Graham C Walker; Dmitry M Korzhnev
Journal: Biochemistry Date: 2016-03-24 Impact factor: 3.162

6. Identification of Small Molecule Translesion Synthesis Inhibitors That Target the Rev1-CT/RIR Protein-Protein Interaction.

Authors: Vibhavari Sail; Alessandro A Rizzo; Nimrat Chatterjee; Radha C Dash; Zuleyha Ozen; Graham C Walker; Dmitry M Korzhnev; M Kyle Hadden
Journal: ACS Chem Biol Date: 2017-06-09 Impact factor: 5.100

A stapled POL κ peptide targets REV1 to inhibit mutagenic translesion synthesis.

1. Stapled peptides for intracellular drug targets.

2. A Small Molecule Targeting Mutagenic Translesion Synthesis Improves Chemotherapy.

3. XRCC1 interaction with the REV1 C-terminal domain suggests a role in post replication repair.

Review 4. Targeting the Translesion Synthesis Pathway for the Development of Anti-Cancer Chemotherapeutics.

5. Interaction between the Rev1 C-Terminal Domain and the PolD3 Subunit of Polζ Suggests a Mechanism of Polymerase Exchange upon Rev1/Polζ-Dependent Translesion Synthesis.

6. Identification of Small Molecule Translesion Synthesis Inhibitors That Target the Rev1-CT/RIR Protein-Protein Interaction.

7. Error-prone translesion synthesis mediates acquired chemoresistance.

8. Suppression of Rev3, the catalytic subunit of Pol{zeta}, sensitizes drug-resistant lung tumors to chemotherapy.

9. Inhibition of oncogenic Wnt signaling through direct targeting of β-catenin.

10. Activation of apoptosis in vivo by a hydrocarbon-stapled BH3 helix.

1. Mechanism of nucleotide discrimination by the translesion synthesis polymerase Rev1.

Review 2. Translesion synthesis inhibitors as a new class of cancer chemotherapeutics.