Kai Ge

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Acting Branch Chief

National Institutes of Health

United States

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About

Dr. Kai Ge is the Acting Branch Chief at the National Institutes of Health, USA. His research focuses on histone methyltransferases, gene expression regulation, and the mechanisms of various cancers. Recent publications include studies on MLL3 and MLL4's roles in platelet production, the implications of H3K36 methylation in cellular plasticity, and the interaction of KMT2D with TGF-β signaling in pancreatic cancer. His work contributes significantly to understanding embryonic development and oncogenic processes in diverse cancer types.

Recent Grants

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Enhancer regulation by H3K4 methyltransferase MLL4/KMT2D and associated factors

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Epigenomic regulation of adipogenesis and adipose expansion

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Articles (11)

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2025

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2024

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2024

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2024

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2024

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2023

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2023

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2023

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2023

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2023

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2023

Collaborators (6)

Young-Kwon Park

National Institutes of Health

UNITED STATES

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Trudy G. Oliver

Duke University

UNITED STATES

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Jiaqi Shi

Associate Professor

University of Michigan

UNITED STATES

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Karl Shpargel

Associate Professor

University of North Carolina

UNITED STATES

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Margarida Almeida Santos

Associate Professor

The University of Texas MD Anderson Cancer Center

UNITED STATES

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Taiping Chen

Professor

The University of Texas MD Anderson Cancer Center

UNITED STATES

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Kai Ge

Research Interests

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About

Recent Grants

Articles (11)

Histone lysine methyltransferases MLL3 and MLL4 direct gene expression to produce platelets efficiently

ASXLs binding to the PHD2/3 fingers of MLL4 provides a mechanism for the recruitment of BAP1 to active enhancers.

MLL4 binds TET3.

BRD4 binds to active cranial neural crest enhancers to regulate RUNX2 activity during osteoblast differentiation

Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis.

MLL3/MLL4 methyltransferase activities control early embryonic development and embryonic stem cell differentiation in a lineage-selective manner

BET Inhibitors Target the SCLC-N Subtype of Small-Cell Lung Cancer by Blocking NEUROD1 Transactivation

KMT2D links TGF-β signaling to noncanonical activin pathway and regulates pancreatic cancer cell plasticity

KMT2D suppresses Sonic hedgehog-driven medulloblastoma progression and metastasis.

KDM6B protects T-ALL cells from NOTCH1-induced oncogenic stress.

Lysine methyltransferase Kmt2d regulates naive CD8<sup>+</sup> T cell activation-induced survival.

Collaborators (6)

Young-Kwon Park

Trudy G. Oliver

Jiaqi Shi

Karl Shpargel

Margarida Almeida Santos

Taiping Chen

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