Molecular regulation of MCU: Implications in physiology and disease

Neeharika Nemani; Santhanam Shanmughapriya; Muniswamy Madesh

doi:10.1016/j.ceca.2018.06.006

Molecular regulation of MCU: Implications in physiology and disease

Neeharika Nemani, Santhanam Shanmughapriya, Muniswamy Madesh

Division of Cardiology

Research output: Contribution to journal › Review article › peer-review

97 Scopus citations

Abstract

Ca ²⁺ flux across the inner mitochondrial membrane (IMM) regulates cellular bioenergetics, intra-cellular cytoplasmic Ca ²⁺ signals, and various cell death pathways. Ca ²⁺ entry into the mitochondria occurs due to the highly negative membrane potential (ΔΨ _m ) through a selective inward rectifying MCU channel. In addition to being regulated by various mitochondrial matrix resident proteins such as MICUs, MCUb, MCUR1 and EMRE, the channel is transcriptionally regulated by upstream Ca ²⁺ cascade, post transnational modification and by divalent cations. The mode of regulation either inhibits or enhances MCU channel activity and thus regulates mitochondrial metabolism and cell fate.

Original language	English (US)
Pages (from-to)	86-93
Number of pages	8
Journal	Cell Calcium
Volume	74
DOIs	https://doi.org/10.1016/j.ceca.2018.06.006
State	Published - Sep 2018

Keywords

Calcium
Channel
EMRE
MCU
MCUR1
MCUb
MICU1
Magnesium
MiST
Miro1
Mitochondria
Oxidants
SLC25A23

ASJC Scopus subject areas

Physiology
Molecular Biology
Cell Biology

Access to Document

10.1016/j.ceca.2018.06.006

Cite this

@article{e43390b6db5f420b94a3105c78e50cb9,

title = "Molecular regulation of MCU: Implications in physiology and disease",

abstract = " Ca 2+ flux across the inner mitochondrial membrane (IMM) regulates cellular bioenergetics, intra-cellular cytoplasmic Ca 2+ signals, and various cell death pathways. Ca 2+ entry into the mitochondria occurs due to the highly negative membrane potential (ΔΨ m ) through a selective inward rectifying MCU channel. In addition to being regulated by various mitochondrial matrix resident proteins such as MICUs, MCUb, MCUR1 and EMRE, the channel is transcriptionally regulated by upstream Ca 2+ cascade, post transnational modification and by divalent cations. The mode of regulation either inhibits or enhances MCU channel activity and thus regulates mitochondrial metabolism and cell fate.",

keywords = "Calcium, Channel, EMRE, MCU, MCUR1, MCUb, MICU1, Magnesium, MiST, Miro1, Mitochondria, Oxidants, SLC25A23",

author = "Neeharika Nemani and Santhanam Shanmughapriya and Muniswamy Madesh",

note = "Publisher Copyright: {\textcopyright} 2018 Elsevier Ltd",

year = "2018",

month = sep,

doi = "10.1016/j.ceca.2018.06.006",

language = "English (US)",

volume = "74",

pages = "86--93",

journal = "Cell Calcium",

issn = "0143-4160",

publisher = "Elsevier Ltd",

}

TY - JOUR

T1 - Molecular regulation of MCU

T2 - Implications in physiology and disease

AU - Nemani, Neeharika

AU - Shanmughapriya, Santhanam

AU - Madesh, Muniswamy

PY - 2018/9

Y1 - 2018/9

N2 - Ca 2+ flux across the inner mitochondrial membrane (IMM) regulates cellular bioenergetics, intra-cellular cytoplasmic Ca 2+ signals, and various cell death pathways. Ca 2+ entry into the mitochondria occurs due to the highly negative membrane potential (ΔΨ m ) through a selective inward rectifying MCU channel. In addition to being regulated by various mitochondrial matrix resident proteins such as MICUs, MCUb, MCUR1 and EMRE, the channel is transcriptionally regulated by upstream Ca 2+ cascade, post transnational modification and by divalent cations. The mode of regulation either inhibits or enhances MCU channel activity and thus regulates mitochondrial metabolism and cell fate.

AB - Ca 2+ flux across the inner mitochondrial membrane (IMM) regulates cellular bioenergetics, intra-cellular cytoplasmic Ca 2+ signals, and various cell death pathways. Ca 2+ entry into the mitochondria occurs due to the highly negative membrane potential (ΔΨ m ) through a selective inward rectifying MCU channel. In addition to being regulated by various mitochondrial matrix resident proteins such as MICUs, MCUb, MCUR1 and EMRE, the channel is transcriptionally regulated by upstream Ca 2+ cascade, post transnational modification and by divalent cations. The mode of regulation either inhibits or enhances MCU channel activity and thus regulates mitochondrial metabolism and cell fate.

KW - Calcium

KW - Channel

KW - EMRE

KW - MCU

KW - MCUR1

KW - MCUb

KW - MICU1

KW - Magnesium

KW - MiST

KW - Miro1

KW - Mitochondria

KW - Oxidants

KW - SLC25A23

UR - http://www.scopus.com/inward/record.url?scp=85049352289&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85049352289&partnerID=8YFLogxK

U2 - 10.1016/j.ceca.2018.06.006

DO - 10.1016/j.ceca.2018.06.006

M3 - Review article

C2 - 29980025

AN - SCOPUS:85049352289

SN - 0143-4160

VL - 74

SP - 86

EP - 93

JO - Cell Calcium

JF - Cell Calcium

ER -

Molecular regulation of MCU: Implications in physiology and disease

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this