Phosphoproteomic Analysis Defines BABAM1 as mTORC2 Downstream Effector Promoting DNA Damage Response in Glioblastoma Cells-Reference-Cited by-同舟云学术

Phosphoproteomic Analysis Defines BABAM1 as mTORC2 Downstream Effector Promoting DNA Damage Response in Glioblastoma Cells

Published:2022-10-31 Issue:12 Volume:21 Page:2893-2904
ISSN:1535-3893
Container-title:Journal of Proteome Research
language:en
Short-container-title:J. Proteome Res.

Author:

Kalpongnukul Nuttiya¹²,Bootsri Rungnapa²³,Wongkongkathep Piriya²⁴,Kaewsapsak Pornchai³⁵,Ariyachet Chaiyaboot³⁶^ORCID,Pisitkun Trairak²⁴^ORCID,Chantaravisoot Naphat²³^ORCID

Affiliation:

1. Interdisciplinary Program of Biomedical Sciences, Graduate School, Chulalongkorn University, Bangkok 10330, Thailand

2. Center of Excellence in Systems Biology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

3. Department of Biochemistry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

4. Research Affairs, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

5. Research Unit of Systems Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

6. Center of Excellence in Hepatitis and Liver Cancer, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

Funder

National Research Council of Thailand

Thailand Research Fund

Institute for the Promotion of Teaching Science and Technology

Chulalongkorn University

Development and Promotion of Science and Technology

Office of the Higher Education Commission

Publisher

American Chemical Society (ACS)

Subject

General Chemistry,Biochemistry

Link

https://pubs.acs.org/doi/pdf/10.1021/acs.jproteome.2c00240

Reference33 articles.

1. Symptom management of brain tumor patients

2. mTOR signaling in glioblastoma: lessons learned from bench to bedside

3. mTORC2 in the center of cancer metabolic reprogramming

4. mTOR signaling at a glance

5. PP242 Counteracts Glioblastoma Cell Proliferation, Migration, Invasiveness and Stemness Properties by Inhibiting mTORC2/AKT

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