Flagship Project

Mindin-integrin-STAT3 signaling and keratinocyte stemness

What keeps me interested in this project is that it asks a very direct cell-state question: what does it take for epidermal cells to hold onto stemness, and how much of that decision is shaped by signals coming from outside the cell?

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Overview

Why this project matters

I have always found stemness questions compelling when they stop being abstract and become about the local conditions that let a state persist. In this project, that meant thinking seriously about extracellular matrix context and integrin behavior, not only about internal factors.

The Mindin-integrin-STAT3 axis gave the project a very concrete path into that problem. What interested me was how extracellular cues are routed through trafficking and downstream transcriptional activation to support the maintenance of an epidermal state.

Core Questions

The questions that kept the project alive for me

How is stemness sustained?

I kept coming back to how epidermal cells preserve a stem or progenitor-like state once they are placed in a particular extracellular and signaling environment.

Why do trafficking and signaling matter together?

What made the problem interesting was that trafficking did not feel like a background process. It looked more like part of the signaling architecture itself.

Why is this broadly relevant?

Questions about how states are stabilized in epidermal systems matter well beyond one pathway. They speak to regeneration, plasticity, and disease-associated persistence.

Approach

Experimental frame

I approached this as a signaling problem that had to stay grounded in cell state. That meant keeping extracellular components, trafficking behavior, and downstream activation in the same frame instead of treating them as separate stories.

In that sense, the project reinforces a broader idea running through my work: epidermal states are not simply maintained from within. They are actively shaped by the environment around them.

Associated Outputs

Where this work appears

Primary Output

2026 Cell Communication and Signaling article

Mindin-mediated αM-integrin endocytosis activates STAT3 to maintain keratinocyte stemness.

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Related Prior Work

2022 Cell Reports paper

Earlier work in this broader signaling area identified an autocrine Snail-Mindin loop supporting epithelial stem or progenitor-like states.

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Portfolio Role

A signaling-centered complement to repair biology

For me, this thread broadens the portfolio from wound-response mechanics into stemness maintenance, extracellular context, and epidermal plasticity.

DNMT3A mechanotransduction

A wound-repair project on how physical cues regulate the localization of an epigenetic regulator.

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Vitiligo spatial transcriptomics

A translational tissue-analysis project on therapy-associated immune remodeling in patient skin.

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Academic profile

Return to the full research overview, publication record, talks, and contact details.

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Contact

Interested in signaling, stemness, and epidermal plasticity?

I am especially interested in research settings that connect skin epithelial biology, state maintenance, signaling logic, and regenerative systems, and I am always glad to talk with people thinking along similar lines.

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