NDLI: Convergent Ca2+ and Zn2+ signaling regulates apoptotic Kv2.1 K+ currents

Content Provider	PubMed Central
Author	Mccord, Meghan C. Aizenman, Elias
Abstract	A simultaneous increase in cytosolic Zn2+ and Ca2+ accompanies the initiation of neuronal cell death signaling cascades. However, the molecular convergence points of cellular processes activated by these cations are poorly understood. Here, we show that Ca2+-dependent activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) is required for a cell death-enabling process previously shown to also depend on Zn2+. We have reported that oxidant-induced intraneuronal Zn2+ liberation triggers a syntaxin-dependent incorporation of Kv2.1 voltage-gated potassium channels into the plasma membrane. This channel insertion can be detected as a marked enhancement of delayed rectifier K+ currents in voltage clamp measurements observed at least 3 h following a short exposure to an apoptogenic stimulus. This current increase is the process responsible for the cytoplasmic loss of K+ that enables protease and nuclease activation during apoptosis. In the present study, we demonstrate that an oxidative stimulus also promotes intracellular Ca2+ release and activation of CaMKII, which, in turn, modulates the ability of syntaxin to interact with Kv2.1. Pharmacological or molecular inhibition of CaMKII prevents the K+ current enhancement observed following oxidative injury and, importantly, significantly increases neuronal viability. These findings reveal a previously unrecognized cooperative convergence of Ca2+- and Zn2+-mediated injurious signaling pathways, providing a potentially unique target for therapeutic intervention in neurodegenerative conditions associated with oxidative stress.
Related Links	http://dx.doi.org/10.1073/pnas.1306238110
Ending Page	13993
Page Count	6
Starting Page	13988
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	34
Volume Number	110
Language	English
Publisher	National Academy of Sciences
Publisher Date	2013-08-20
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Convergent $Ca^{2+}$ and $Zn^{2+}$ signaling regulates apoptotic Kv2.1 $K^{+}$ currents

Apoptotic surge of potassium currents is mediated by p38 phosphorylation of Kv2.1

Syntaxin-binding domain of Kv2.1 is essential for the expression of apoptotic K+ currents

Zn2+ regulates Kv2.1 voltage-dependent gating and localization following ischemia

A Ca2+ signaling pathway regulates a K+ channel for low-K response in Arabidopsis

Regulation of Pro-Apoptotic Phosphorylation of Kv2.1 K+ Channels

Coupled Ca2+/H+ transport by cytoplasmic buffers regulates local Ca2+ and H+ ion signaling

Developmental regulation of Ca2+ and K+ currents during hormone-induced maturation of starfish oocytes.

Inhibition of protein synthesis prolongs Ca2+-mediated reduction of K+ currents in molluscan neurons.

Convergent Ca2+ and Zn2+ signaling regulates apoptotic Kv2.1 K+ currents

Similar Documents

Convergent $Ca^{2+}$ and $Zn^{2+}$ signaling regulates apoptotic Kv2.1 $K^{+}$ currents

Apoptotic surge of potassium currents is mediated by p38 phosphorylation of Kv2.1

Syntaxin-binding domain of Kv2.1 is essential for the expression of apoptotic K+ currents

Zn2+ regulates Kv2.1 voltage-dependent gating and localization following ischemia

A Ca2+ signaling pathway regulates a K+ channel for low-K response in Arabidopsis

Regulation of Pro-Apoptotic Phosphorylation of Kv2.1 K+ Channels

Coupled Ca2+/H+ transport by cytoplasmic buffers regulates local Ca2+ and H+ ion signaling

Developmental regulation of Ca2+ and K+ currents during hormone-induced maturation of starfish oocytes.

Inhibition of protein synthesis prolongs Ca2+-mediated reduction of K+ currents in molluscan neurons.

Convergent Ca2+ and Zn2+ signaling regulates apoptotic Kv2.1 K+ currents