Cornell Researchers Discover New Protein Interaction That Balances Cellular Recycling System

The findings show an interaction between two proteins that helps regulate a critical cellular process with implications for diseases like cancer and neurodegenerative disorders.

Published on Feb. 10, 2026

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Cornell researchers have discovered a new way cells regulate how they respond to stress, identifying an interaction between two proteins that helps keep a critical cellular recycling system in balance. The study found that a protein called SHKBP1 regulates another protein, p62, which plays a key role in clearing damaged cell components and activating antioxidant defenses. By helping maintain this balance, SHKBP1 allows cells to respond appropriately to stress - a process that can break down in diseases such as cancer and neurodegenerative disorders.

Why it matters

Understanding how SHKBP1 influences the balance between p62 activity and the cell's antioxidant response could open new therapeutic avenues. If loss of SHKBP1 function naturally boosts the antioxidant response, perhaps drugs that safely inhibit SHKBP1 could provide neuroprotection in diseases like Alzheimer's and Parkinson's. Conversely, cancer cells often hijack this pathway to survive, so targeting SHKBP1 could potentially weaken that survival mechanism.

The details

The study, published in the Journal of Cell Biology, found that SHKBP1 binds directly to a portion of p62 that normally allows it to aggregate into large clusters. This SHKBP1 binding physically prevents p62 molecules from clustering together into large 'p62 bodies'. Removing SHKBP1 caused these p62 bodies to grow larger and less fluid, while adding extra SHKBP1 made them smaller and more dynamic. This balance that SHKBP1 helps maintain is crucial, as too little p62 activity can allow toxic proteins to accumulate, while too much p62 activity can fuel tumor growth in cancer.

  • The study was published on February 6, 2026.

The players

Lin Luan

A doctoral candidate in the Department of Biochemistry, Molecular and Cell Biology at Cornell University and lead author of the study.

Jeremy Baskin

Associate professor and Nancy and Peter Meinig Family Investigator in the Life Sciences in the Department of Chemistry and Chemical Biology at Cornell University and the Weill Institute for Cell and Molecular Biology, and senior author of the study.

SHKBP1

A protein that regulates another protein called p62, which plays a key role in clearing damaged cell components and activating antioxidant defenses.

p62

A protein that gathers damaged proteins into compartments called 'p62 bodies' where they can be dealt with. It plays a central role in the cell's recycling operation.

Keap1–Nrf2 pathway

A well-known antioxidant defense system that cells rely on to respond to oxidative stress. p62 helps remove a protein that suppresses this protective response.

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What they’re saying

“Our cells are constantly dealing with stresses, whether from normal metabolism or specific insults from the environment. A protein called p62 is a central player in this recycling operation, as it gathers damaged proteins into compartments called 'p62 bodies' where they can be dealt with.”

— Jeremy Baskin, Associate professor and Nancy and Peter Meinig Family Investigator in the Life Sciences (Journal of Cell Biology)

“What we found was that SHKBP1 binds directly to a portion of p62 that normally allows it to aggregate into large clusters, so SHKBP1 binding physically prevented p62 molecules from clustering together into large bodies. Removing SHKBP1 caused p62 bodies to grow larger and less fluid, while adding extra SHKBP1 made them smaller and more dynamic.”

— Jeremy Baskin, Associate professor and Nancy and Peter Meinig Family Investigator in the Life Sciences (Journal of Cell Biology)

“Understanding how SHKBP1 influences this balance could open new therapeutic avenues. If loss of SHKBP1 function naturally boosts the Nrf2 response, perhaps we could develop drugs that safely inhibit SHKBP1 in the brain to provide neuroprotection.”

— Jeremy Baskin, Associate professor and Nancy and Peter Meinig Family Investigator in the Life Sciences (Journal of Cell Biology)

What’s next

The researchers plan to further investigate how the SHKBP1-p62 interaction influences the Keap1-Nrf2 antioxidant defense pathway and explore potential therapeutic applications in diseases like cancer and neurodegenerative disorders.

The takeaway

This discovery of a new protein interaction that helps regulate a critical cellular recycling system could lead to new strategies for targeting diseases where this balance breaks down, such as cancer and neurodegenerative disorders. Understanding how to modulate the SHKBP1-p62 interaction may open up new avenues for therapeutic intervention.