Targeting “Undruggable” Proteins Opens New Doors for Neurodegenerative Disease Treatment

Publication date: Feb 20, 2024

By preventing Keap1 from marking Nrf2 for degradation, Nrf2 accumulates in the nucleus, activating the Antioxidant Response Element (ARE) and driving the expression of detoxifying and antioxidant genes. The promise lies in the development of a new modality for the design of therapeutics. Subscribe to Technology Networks daily newsletter, delivering breaking science news straight to your inbox every day. 2024:2311467. doi: 10. 1002/adma. 202311467This article has been republished from the following materials. Inhibiting the Keap1/Nrf2 protein-protein interaction with protein-like polymers. This study is just the beginning. Note: material may have been edited for length and content.

Concepts Keywords
Biochemistry Antioxidant
Neurodegenerative Cellular
Polymersplps Disease
Wisconsinmadison Diseases
Gianneschi
Interaction
Johnson
Keap1
Nds
Neurodegenerative
Nrf2
Oxidative
Professor
Protein
Stress

Semantics

Type Source Name
disease MESH Neurodegenerative Disease
pathway REACTOME Neurodegenerative Diseases
disease MESH Amyotrophic lateral sclerosis
pathway KEGG Amyotrophic lateral sclerosis
disease MESH oxidative stress
disease MESH amyloid plaques
drug DRUGBANK Pyridoxal Phosphate
drug DRUGBANK Nonoxynol-9

Original Article

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