Potent Inhibition of HIF1α and p300 Interaction by a Constrained Peptide Derived from CITED2-Reference-Cited by-同舟云学术

Potent Inhibition of HIF1α and p300 Interaction by a Constrained Peptide Derived from CITED2

Published:2021-09-02 Issue:18 Volume:64 Page:13693-13703
ISSN:0022-2623
Container-title:Journal of Medicinal Chemistry
language:en
Short-container-title:J. Med. Chem.

Author:

Qin Xuan¹,Chen Hailing¹,Tu Licheng¹,Ma Yue¹,Liu Na²,Zhang Haowei³,Li Di¹,Riedl Bernd⁴,Bierer Donald⁴,Yin Feng²,Li Zigang¹²^ORCID

Affiliation:

1. State Key Laboratory of Chemical Oncogenomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China

2. Pingshan Translational Medicine Center, Shenzhen Bay Laboratory, Shenzhen 518055, China

3. Key Lab in Healthy Science and Technology, Division of Life Science, Shenzhen Graduate School of Tsinghua University, Shenzhen 518055, China

4. Department of Medicinal Chemistry, Bayer AG, Aprather Weg 18A, Wuppertal 42096, Germany

Funder

Ministry of Science and Technology of the People's Republic of China

China Postdoctoral Science Foundation

National Natural Science Foundation of China

Natural Science Foundation of Guangdong Province

Shenzhen-Hong Kong Institute of Brain Science

Shenzhen Science and Technology Innovation Committee

Beijing National Laboratory of Molecular Science

Publisher

American Chemical Society (ACS)

Subject

Drug Discovery,Molecular Medicine

Link

https://pubs.acs.org/doi/pdf/10.1021/acs.jmedchem.1c01043

Reference58 articles.

1. Reprogramming of the Tumor in the Hypoxic Niche: The Emerging Concept and Associated Therapeutic Strategies

2. Hypoxia inducible factor (HIF) as a model for studying inhibition of protein–protein interactions

3. HIF1α and HIF2α: sibling rivalry in hypoxic tumour growth and progression

4. A RNA antagonist of hypoxia-inducible factor-1α, EZN-2968, inhibits tumor cell growth

5. Flavopiridol downregulates hypoxia-mediated hypoxia-inducible factor-1α expression in human glioma cells by a proteasome-independent pathway: Implications for in vivo therapy

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