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Jiyang Cai

Researcher at University of Texas Medical Branch

Publications -  82
Citations -  17334

Jiyang Cai is an academic researcher from University of Texas Medical Branch. The author has contributed to research in topics: Oxidative stress & Apoptosis. The author has an hindex of 36, co-authored 78 publications receiving 15716 citations. Previous affiliations of Jiyang Cai include Yale University & Emory University.

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Journal ArticleDOI

Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked

Jie Yang, +10 more
- 21 Feb 1997 - 
TL;DR: One possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria, which is normally located in the mitochondrial intermembrane space.
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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore

Jason E. Kokoszka, +13 more
- 29 Jan 2004 - 
TL;DR: It is shown that mitochondria lacking ANT could still be induced to undergo permeability transition, resulting in release of cytochrome c.
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Superoxide in apoptosis. Mitochondrial generation triggered by cytochrome c loss

Jiyang Cai, +1 more
- 08 May 1998 - 
TL;DR: Bcl-2, a protein that protects against apoptosis and blocks cytochrome c release, prevents superoxide production when it is overexpressed, and provides a mechanism for redox signaling that is concomitant with cy tochrome c-dependent activation of caspases.
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Mitochondrial control of apoptosis: the role of cytochrome c.

Jiyang Cai, +2 more
- 10 Aug 1998 - 
TL;DR: Anti-apoptotic Bcl-2 family proteins function as gatekeepers to prevent the release of both cyt c and AIF and may also be involved in the direct binding of Apaf molecules as regulatory elements further downstream from the mitochondrial apoptotic signals.