Identification of a novel BCL2-specific inhibitor that binds predominantly to the BH1 domain-Reference-Cited by-同舟云学术

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Identification of a novel BCL2-specific inhibitor that binds predominantly to the BH1 domain

Published:2016-08-17 Issue:18 Volume:283 Page:3408-3437
ISSN:1742-464X
Container-title:The FEBS Journal
language:en
Short-container-title:FEBS J

Author:

Iyer Divyaanka¹,Vartak Supriya V.¹,Mishra Archita²,Goldsmith Gunaseelan³,Kumar Sujeet⁴,Srivastava Mrinal¹,Hegde Mahesh¹,Gopalakrishnan Vidya¹³,Glenn Mark⁵,Velusamy Mahesh³,Choudhary Bibha³,Kalakonda Nagesh⁵,Karki Subhas S.⁴,Surolia Avadhesha²,Raghavan Sathees C.¹

Affiliation:

1. Department of Biochemistry; Indian Institute of Science; Bangalore India

2. Molecular Biophysics Unit; Indian Institute of Science; Bangalore India

3. Institute of Bioinformatics and Applied Biotechnology, Electronics City; Bangalore India

4. Department of Pharmaceutical Chemistry; KLE University's College of Pharmacy; Bangalore India

5. Haematology; Department of Molecular and Clinical Cancer Medicine University of Liverpool; UK

Funder

Leukemia Research Foundation

Indian Institute of Science

Council of Scientific and Industrial Research

All India Council for Technical Education

Department of Electronics and Information Technology, Ministry of Communications and Information Technology

Department of IT, BT and S&T, Government of Karnataka, India

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Biochemistry

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1111/febs.13815/fullpdf

Reference58 articles.

1. Apoptosis and cancer: the genesis of a research field;Cotter;Nat Rev Cancer,2009

2. Organelle-specific initiation of cell death pathways;Ferri;Nat Cell Biol,2001

3. Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak;Willis;Science,2007

4. BCL-2 family members and the mitochondria in apoptosis;Gross;Genes Dev,1999

5. Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from an androgen-dependent to an androgen-independent growth stage;Lin;Cell Res,2007

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