Tumor suppressor p53 induces miR-1915 processing to inhibit Bcl-2 in the apoptotic response to DNA damage

Author:

Nakazawa Kazuya12,Dashzeveg Nurmaa12,Yoshida Kiyotsugu1

Affiliation:

1. Department of Biochemistry; The Jikei University School of Medicine; Tokyo Japan

2. Medical Research Institute; Tokyo Medical and Dental University; Japan

Funder

Astellas Foundation for Research on Medical Resources

Japan Foundation for Applied Enzymology

Mochida Memorial Foundation for Medical and Pharmaceutical Research

NOVARTIS Foundation for the Promotion of Science

Project Mirai Cancer Research Grants

Sumitomo Foundation

Suzuken Memorial Foundation

Takeda Science Foundation

The Jikei University Graduate Research Fund

The Ministry of Education, Science and Culture of Japan

Uehara Memorial Foundation

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference32 articles.

1. Bcl-2 blocks apoptosis in cells lacking mitochondrial DNA;Jacobson;Nature,1993

2. Programmed cell death: Bcl-2;Korsmeyer;In Important Adv Oncol 1993,1993

3. Regulation by bcl-2, c-myc, and p53 of susceptibility to induction of apoptosis by heat shock and cancer chemotherapy compounds in differentiation-competent and -defective myeloid leukemic cells;Lotem;Cell Growth Differ,1993

4. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death;Oltvai;Cell,1993

5. Bcl-2 family proteins: regulators of apoptosis and chemoresistance in hematologic malignancies;Reed;Semin Hematol,1997

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