当前位置： SCI文献检索 > PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA期刊下所有文献 > A splicing variant of a death domain protein that is regulated by a mitogen-activated kinase is a substrate for c-Jun N-terminal kinase in the human central nervous system.

A splicing variant of a death domain protein that is regulated by a mitogen-activated kinase is a substrate for c-Jun N-terminal kinase in the human central nervous system.

Abstract：

:The mitogen-activated kinase activating death domain protein (MADD) that is differentially expressed in neoplastic vs. normal cells (DENN) was identified as a substrate for c-Jun N-terminal kinase 3, the first demonstration of such an activity for this stress-activated kinase that is predominantly expressed in the brain. A splice isoform was identified that is a variant of MADD. A protein identical to MADD has been reported to be expressed differentially in neoplastic vs. normal cells and is termed "DENN." We demonstrated differential effects on DENN/MADD in a stressed vs. basal environment. Using in situ hybridization, we localized both the substrate and the kinase to large pyramidal neurons in the human hippocampus. It was interesting that, in four of four patients with neuropathologically confirmed acute hypoxic changes, we detected a unique translocation of DENN/MADD to the nucleolus. These changes were apparent only in neurons sensitive to hypoxia. Moreover, in those cells, translocation of the substrate was accompanied by nuclear translocation of JNK3. These findings place DENN/MADD and JNK in important hypoxia insult-induced intracellular signaling pathways. Our conclusions are important for future studies for understanding these stress-activated mechanisms.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Zhang Y,Zhou L,Miller CA

doi

10.1073/pnas.95.5.2586

subject

Has Abstract

pub_date

1998-03-03 00:00:00

pages

2586-91

issue

5

eissn

0027-8424

issn

1091-6490

journal_volume

95

pub_type

杂志文章

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