The metabolic reprogramming and vulnerability of SF3B1 mutations

W. Brian Dalton

doi:10.1080/23723556.2019.1697619

The metabolic reprogramming and vulnerability of SF3B1 mutations

W. Brian Dalton

School of Medicine

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

Mutations in the splicing factor 3b subunit 1 (SF3B1) gene create a neomorphic protein that disrupts RNA splicing, but the downstream consequences of this missplicing are unclear. Our recent study of isogenic human cells demonstrated that SF3B1^MUT induces reprogramming of energy metabolism and a targetable vulnerability to deprivation of the nonessential amino acid serine.

Original language	English (US)
Article number	1697619
Journal	Molecular and Cellular Oncology
Volume	7
Issue number	3
DOIs	https://doi.org/10.1080/23723556.2019.1697619
State	Published - May 3 2020

Keywords

PHGDH
SF3B1
metabolism
serine
spliceosome

ASJC Scopus subject areas

Molecular Medicine
Cancer Research

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10.1080/23723556.2019.1697619

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abstract = "Mutations in the splicing factor 3b subunit 1 (SF3B1) gene create a neomorphic protein that disrupts RNA splicing, but the downstream consequences of this missplicing are unclear. Our recent study of isogenic human cells demonstrated that SF3B1MUT induces reprogramming of energy metabolism and a targetable vulnerability to deprivation of the nonessential amino acid serine.",

keywords = "PHGDH, SF3B1, metabolism, serine, spliceosome",

author = "Dalton, {W. Brian}",

note = "Funding Information: SF3B1 spliceosome serine PHGDH metabolism U.S. Department of Defense 10.13039/100000005 W81XWH-17-1-0035 This work was supported by the Eli Lilly and Company;U.S. Department of Defense [W81XWH-17-1-0035]. Publisher Copyright: {\textcopyright} 2020, {\textcopyright} 2020 The Author(s). Published with license by Taylor & Francis Group, LLC.",

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AB - Mutations in the splicing factor 3b subunit 1 (SF3B1) gene create a neomorphic protein that disrupts RNA splicing, but the downstream consequences of this missplicing are unclear. Our recent study of isogenic human cells demonstrated that SF3B1MUT induces reprogramming of energy metabolism and a targetable vulnerability to deprivation of the nonessential amino acid serine.

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KW - metabolism

KW - serine

KW - spliceosome

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The metabolic reprogramming and vulnerability of SF3B1 mutations

Abstract

Keywords

ASJC Scopus subject areas

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