Basil Hubbard

Associate Professor

University of Toronto

Canada

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About

Dr. Basil Hubbard is an Associate Professor at the University of Toronto, Canada. His research focuses on cancer drug discovery and treatment using CRISPR/Cas technologies, as well as the pharmacology of nucleoside transporters and oxidative phosphorylation vulnerabilities in cancer. He has published extensively on topics including tumor suppressor regulation, metabolic stress in cancer, and innovative gene editing techniques.

Articles (11)

Year:

2025

Year:

2024

Year:

2024

Year:

2024

Year:

2023

Year:

2022

Year:

2022

Year:

2022

Year:

2022

Year:

2021

Year:

2020

Collaborators (10)

James Hammond

University of Alberta

CANADA

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Mark McDermott

Professor

University of Alberta

CANADA

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John Klassen

University of Alberta

CANADA

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Richard Schulz

Professor

University of Alberta

CANADA

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John R. Ussher

CANADA

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Evangelos D. Michelakis

University of Alberta

CANADA

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Olivier Julien

Associate Professor

University of Alberta

CANADA

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Rony Pain

University of Alberta

CANADA

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Mohammad Ali

Assistant Professor

Binghamton University

UNITED STATES

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Juli Gibbs

Associate Professor

University of Alberta

CANADA

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Basil Hubbard

Research Interests

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About

Articles (11)

CRISPR/Cas technologies for cancer drug discovery and treatment

MMP‐2 regulates Src activation via repression of the CHK/MATK tumor suppressor in osteosarcoma

Multiomics analysis identifies oxidative phosphorylation as a cancer vulnerability arising from myristoylation inhibition

Development of a Novel HEK293 Cell Model Lacking <i>SLC29A1</i> to Study the Pharmacology of Endogenous <i>SLC29A2</i>-Encoded Equilibrative Nucleoside Transporter Subtype 2.

Reversible and irreversible inhibitors of coronavirus Nsp15 endoribonuclease

CRISPR-Click Enables Dual-Gene Editing with Modular Synthetic sgRNAs

A reversible metabolic stress-sensitive regulation of CRMP2A orchestrates EMT/stemness and increases metastatic potential in cancer.

Guide RNAs containing universal bases enable Cas9/Cas12a recognition of polymorphic sequences

Lipid phosphate phosphatase-2 promotes tumor growth through increased c-Myc expression.

Matrix metalloproteinase‐2 mediates ribosomal RNA transcription by cleaving nucleolar histones

A conserved acetylation switch enables pharmacological control of tubby-like protein stability

Collaborators (10)

James Hammond

Mark McDermott

John Klassen

Richard Schulz

John R. Ussher

Evangelos D. Michelakis

Olivier Julien

Rony Pain

Mohammad Ali

Juli Gibbs

Make your next move.

Basil Hubbard

Research Interests

Explore related searches

Contact this professor

About

Articles (11)

CRISPR/Cas technologies for cancer drug discovery and treatment

MMP‐2 regulates Src activation via repression of the CHK/MATK tumor suppressor in osteosarcoma

Multiomics analysis identifies oxidative phosphorylation as a cancer vulnerability arising from myristoylation inhibition

Development of a Novel HEK293 Cell Model Lacking &lt;i&gt;SLC29A1&lt;/i&gt; to Study the Pharmacology of Endogenous &lt;i&gt;SLC29A2&lt;/i&gt;-Encoded Equilibrative Nucleoside Transporter Subtype 2.

Reversible and irreversible inhibitors of coronavirus Nsp15 endoribonuclease

CRISPR-Click Enables Dual-Gene Editing with Modular Synthetic sgRNAs

A reversible metabolic stress-sensitive regulation of CRMP2A orchestrates EMT/stemness and increases metastatic potential in cancer.

Guide RNAs containing universal bases enable Cas9/Cas12a recognition of polymorphic sequences

Lipid phosphate phosphatase-2 promotes tumor growth through increased c-Myc expression.

Matrix metalloproteinase‐2 mediates ribosomal RNA transcription by cleaving nucleolar histones

A conserved acetylation switch enables pharmacological control of tubby-like protein stability

Collaborators (10)

James Hammond

Mark McDermott

John Klassen

Richard Schulz

John R. Ussher

Evangelos D. Michelakis

Olivier Julien

Rony Pain

Mohammad Ali

Juli Gibbs

Make your next move.

Development of a Novel HEK293 Cell Model Lacking <i>SLC29A1</i> to Study the Pharmacology of Endogenous <i>SLC29A2</i>-Encoded Equilibrative Nucleoside Transporter Subtype 2.