Pau Castel

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Assistant Professor

New York University Grossman School of Medicine

United States

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About

Pau Castel is an Assistant Professor at New York University Grossman School of Medicine in the United States. His research focuses on the structural and functional analysis of RAS GTPases, protein degradation mechanisms, and the regulatory roles of angiocrine factors in adiposity. Recent articles by Professor Castel explore the impact of LZTR1 and RIT1 in genetic disorders and cancer biology, highlighting the significance of these pathways in therapeutic discovery.

Recent Grants

Grant: Close

Molecular and Cellular Functions of LZTR1 Mutations in Schwannomatosis

Open Date: 2020-08-01

Close Date: 2022-07-31

Grant: Close

The role of Sin1 in Kras-driven cancer

Open Date: 2020-07-01

Close Date: 2022-06-30

Grant: Close

Novel effectors of oncogenic KRAS that regulate cell signaling

Open Date: 2017-07-01

Close Date: 2020-07-01

Grant: Close

New Ways of Targeting K-Ras

Open Date: 2016-04-01

Close Date: 2023-03-31

Grant: Close

Unraveling resistance to PI3K-alpha inhibitors in breast cancer

Open Date: 2015-08-01

Close Date: 2020-07-31

Articles (11)

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2025

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2022

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2022

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2022

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2022

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2022

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2021

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2021

Year:

2021

Year:

2021

Year:

2021

Collaborators (15)

Alice Cheng

University of California, San Francisco

UNITED STATES

Pau Castel

Research Interests

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About

Recent Grants

Articles (11)

Structural Basis for LZTR1 Recognition of RAS GTPases for Degradation

The seventh international RASopathies symposium: Pathways to a cure-expanding knowledge, enhancing research, and therapeutic discovery.

Angiocrine polyamine production regulates adiposity.

The Oncogenic PI3K-Induced Transcriptomic Landscape Reveals Key Functions in Splicing and Gene Expression Regulation

Cross-species analysis of LZTR1 loss-of-function mutants demonstrates dependency to RIT1 orthologs

Defective protein degradation in genetic disorders

Minor intron retention drives clonal hematopoietic disorders and diverse cancer predisposition.

RAS interaction with Sin1 is dispensable for mTORC2 assembly and activity

The RAS GTPase RIT1 compromises mitotic fidelity through spindle assembly checkpoint suppression.

Josep Baselga (1959-2021).

José Baselga (1959-2021).

Collaborators (15)

Alice Cheng

Elizabeth Pierpont

Emilia Galperin

Michael Trnka

Anatoly Urisman

Sebastián Zagmutt

Maija Kiuru

Pablo M. Garcia-Roves

Eric Wang

Emiliano Cocco

Maria Kontaridis

Laura Herrero

Beth Stronach

Shruti Garg

Anton Bennett

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