Infoscience
metadata only
Slow-Binding and Covalent HDAC Inhibition: A New Paradigm?
The dysregulated post-translational modification of proteins is an established hallmark of human disease. Through Zn2+-dependent hydrolysis of acyl-lysine modifications, histone deacetylases (HDACs) are key regulators of disease-implicated signaling pathways and tractable drug targets in the clinic.
Conceptio Open Archive
Analyze & explore related research in Conceptio
Connect this record directly into your research workflow or AI agent. Explore citations across open repositories, query full text, and export structured proof bundles.
This document is indexed with metadata only: full text is not available in the archive for this record. Open the official source ↗
Related documents
- Potential Role of Sirtuins As Epigenetic Biomarkers of the Patient with Atherosclerosis or Calcific Aortic Stenosis#1111807
- HDAC7 acts as an astrocytic mediator of Aβ pathology that directly engages IKK to drive astrocyte neurotoxicity and neurodegeneration in Alzheimer's disease.#645238
- Integrated Bioinformatic and Experimental Identification of DHCR24 and NRG1 as Key Cellular Aging Genes in Diabetic Cardiomyopathy.#320549
- Long non-coding RNA GAS6-AS1 and its molecular mechanisms in human cancer (Review).#1054072
- Decoding 3D chromatin architecture reveals distinct enhancer classes underlying hierarchical gene regulation in prostate cancer.#396075
Record · ID 1134211
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Bring this data into your agent: Connect via MCP or API · 20 free credits to start · no card required
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive