Related Experiment Video
Updated: May 16, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017
CREB-mediated Bcl-2 expression contributes to RCAN1 protection from hydrogen peroxide-induced neuronal death
Seon Sook Kim1, Shin Ah Jang, Su Ryeon Seo
1Department of Molecular Bioscience, College of Biomedical Science, Institute of Bioscience & Biotechnology, Kangwon National University, Hyoja-dong, Chuncheon 200-701, Republic of Korea.
Abstract:
Regulator of calcineurin 1 (RCAN1) is located on the Down syndrome critical region (DSCR) locus in human chromosome 21. In this study, we investigated the functional role of RCAN1 in the reactive oxygen species (ROS)-mediated neuronal death signaling. We found that RCAN1 was able to protect the cells from H(2)O(2) -induced cytotoxicity. The expression of RCAN1 caused an inhibition of the H(2)O(2) -induced activation of mitogen-activated protein kinases (MAPKs) and AP-1. In contrast, RCAN1 significantly enhanced the activity of cAMP response element-binding protein (CREB). Furthermore, RCAN1 induced the expression of the CREB target gene, Bcl-2. Consistently, knockdown of endogenous RCAN1 using shRNA down regulated the phosphorylation of CREB and the expression of Bcl-2, which protects the cells from H(2)O(2) -induced cytotoxicity. Our data provide a new mechanism for the cytoprotective function of RCAN1 in response to oxidant-induced apoptosis.
More Related Videos
Related Concept Videos
The Intrinsic Apoptotic Pathway
Necrosis
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
The Extrinsic Apoptotic Pathway
Regulation of the Unfolded Protein Response
Caspases

